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\n \n\n \n \n \n \n \n \n Effect of alpha-lactalbumin and lactoferrin oleic acid complexes on chromatin structural organization.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biochemical and Biophysical Research Communications, 520(1): 136-139. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Effect$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 4 downloads\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Delayed Colony Formation in Diploid Cells of Various Genotypes after UV Light Irradiation.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 55(7): 904-907. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Delayed$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Abnormal activity of transcription factors gli in high-grade gliomas.\n \n \n \n \n\n\n \n Volnitskiy, A.; Shtam, T.; Burdakov, V.; Kovalev, R.; Konev, A.; and Filatov, M.\n\n\n \n\n\n\n PLoS ONE, 14(2). 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Abnormal$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Volnitskiy2019,\r\nauthor={Volnitskiy, A. and Shtam, T. and Burdakov, V. and Kovalev, R. and Konev, A. and Filatov, M.},\r\ntitle={Abnormal activity of transcription factors gli in high-grade gliomas},\r\njournal={PLoS ONE},\r\nyear={2019},\r\nvolume={14},\r\nnumber={2},\r\ndoi={10.1371/journal.pone.0211980},\r\nart_number={e0211980},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85061246108&doi=10.1371%2fjournal.pone.0211980&partnerID=40&md5=b33be3ba1c58420838f9b1c65e11c6ae},\r\naffiliation={Petersburg Nuclear Physics Institute named by B.P. Konstantinov of National Research Centre "Kurchatov Institute, Gatchina, Russian Federation; N.N. Petrov National Medical Research Center of Oncology, St. Petersburg, Pesochnyj, Leningradskaya, Russian Federation},\r\nabstract={Malignant transformation is associated with loss of cell differentiation, anaplasia. Transcription factors gli, required for embryonic development, may be involved in this process. We studied the activity of transcription factors gli in high-grade gliomas and their role in maintenance of stem cell state and glioma cell survival. 20 glioma cell lines and a sample of a normal adult brain tissue were used in the present study. We found the expression of gli target genes, including GLI1 and FOXM1, in all tested glioma cell lines, but not in the normal tissue. Interestingly, the expression of gli target genes in some glioma cell lines was observed together with a high level of their transcriptional repressor, Gli3R. Knockdown of GLI3 in one of these lines resulted in decrease of gli target gene expression. These data suggest that Gli3R does not prevent the gli target genes transcription, and gli3 acts in glioma cells more as an activator, than a repressor of transcription. We observed that gli regulated the expression of such genes, as SOX2 or OCT4 that maintain stem cell state, and TET1, involving in DNA demethylation. Treatment with GANT61 or siRNA against GLI1, GLI2, or GLI3 could result in complete glioma cell death, while cyclopamine had a weaker and line-specific effect on glioma cell survival. Thus, the gli transcription factors are abnormally active in high-grade gliomas, regulate expression of genes, maintaining the stem cell state, and contribute to glioma cell survival. © 2019 Volnitskiy et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.},\r\ncorrespondence_address1={Volnitskiy, A.; Petersburg Nuclear Physics Institute named by B.P. Konstantinov, National Research Centre "Kurchatov InstituteRussian Federation; email: voln.a@yandex.ru},\r\npublisher={Public Library of Science},\r\nissn={19326203},\r\ncoden={POLNC},\r\npubmed_id={30730955},\r\nlanguage={English},\r\nabbrev_source_title={PLoS ONE},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The role of the chromatin remodeling factor CHD1 in the global organization of drosophila chromosomes.\n \n \n \n \n\n\n \n Tiutiunnik, A.; Baranovskaya, I.; Kuchins-Kaya, Y.; Gnennaya, Y.; Shalaev, A.; and Konev, A.\n\n\n \n\n\n\n Biopolymers and Cell, 35(3): 174-175. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Tiutiunnik2019174,\r\nauthor={Tiutiunnik, A. and Baranovskaya, I. and Kuchins-Kaya, Y. and Gnennaya, Y. and Shalaev, A. and Konev, A.},\r\ntitle={The role of the chromatin remodeling factor CHD1 in the global organization of drosophila chromosomes},\r\njournal={Biopolymers and Cell},\r\nyear={2019},\r\nvolume={35},\r\nnumber={3},\r\npages={174-175},\r\ndoi={10.7124/bc.0009AE},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85073348930&doi=10.7124%2fbc.0009AE&partnerID=40&md5=4b73aa762c9e7ef6cd358b7bee5a21ac},\r\naffiliation={NRC «Kurchatov Institute»-PNPI, Gatchina, Russian Federation},\r\nabstract={Chromatin is organized into euchromatin and heterochromatin. Drosophila melanogaster also uses two systems of whole chromosome regulation: dosage compensation mediating the two fold up-regulation of male X-linked genes and the Painting of Fourth, regulating heterochromatic 4th chromosome. Both heterochromatin formation and dosage compensation are accompanied by global changes in chromatin structure. Evolutionary conserved cromatin assembly and remodeling factor CHD1 is an euchromatic protein which co-localizes in polytene chromosomes with the RNA polymerase II. The aim of this study was to analyze the role of Drosophila CHD1 in the control of global organization of polytene chromosomes. Methods: To study the action of CHD1 on global chromosome stucture, we examined the consequences of loss of CHD1 and of over-expression ATPase-dead or wild type CHD1 on polytene chromosome organisation in Drosophila larvae salivary glands. Results: In polytene chromosomes deprived of CHD1, we observed a specific bloating, blurring and shortening of the male X chromosome. Morphology of the female X chromosomes does not differ from autosomes and from the morphology of wild type chromosomes. In Chd1 null mutant males, the maternally contributed CHD1 accumulates exclusively in X-chromosome. In the wild type larvae we observed a specific enreachment of the CHD1 on the male X chromosome. Additional bands of CHD1 completely co-localize with the MSL proteins of the Dosage Compensation Complex (DCC), which associates specifically with the male X chromosome. The targeting of the CHD1 on the male X chromosome depends on the presence of a functional DCC. The loss of CHD1 results in preferential male lethality. Chd1 become essential in combination with deletion of one of two genes, encoding variant histone H3.3, His 3.3 B. An effect of Chd1 on male X-chromosome morphology is increased by the His 3.3 B deficiency. GAL4-driven ectopic expression of wild type CHD1 or its ATPase-dead form leads to a strong decompactization of the specific regions of salivary gland polytene chromosomes in euchromatin. Immunostaining with antibodies to CHD1 and elongating RNA polymerase II reveals bright staining at all sites with an altered chromatin structure. Over-expression of wild type CHD1, but not of its ATPase-dead form also results in a strong decondensation of the chromocenter, where pericentric heterochromatin fuses, and of the 4th chromosome. Decondensed heterochromatin is brightly stained with antibodies to CHD1, where CHD1 does not co-localize with RNA Pol II and where heterochromatic protein HP1and histone H1 are lost. Real – time PCR analysis have revealed that the CHD1 over-expression increases the level of replication of X-chromosome heterochromatic repeats 1.688 satellite and Stellate, however does not affect the underreplication of the heterochromatic genes in autosomes. Conclusions: Here we show that the loss or over-expression of CHD1 severely and very specifically affect the global chromatin organization of Drosophila polytene chromosomes. Our finding suggests a new link between the organization of hyperactive chromatin of the male X – chromosome and of transcriptionally silent heterochromatin. © 2019, National Academy of Sciences of Ukraine. All rights reserved.},\r\nfunding_details={Russian Foundation for Basic Research15-04-99583},\r\nfunding_details={Russian Science Foundation19-74-20075},\r\n}

\n

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\n Chromatin is organized into euchromatin and heterochromatin. Drosophila melanogaster also uses two systems of whole chromosome regulation: dosage compensation mediating the two fold up-regulation of male X-linked genes and the Painting of Fourth, regulating heterochromatic 4th chromosome. Both heterochromatin formation and dosage compensation are accompanied by global changes in chromatin structure. Evolutionary conserved cromatin assembly and remodeling factor CHD1 is an euchromatic protein which co-localizes in polytene chromosomes with the RNA polymerase II. The aim of this study was to analyze the role of Drosophila CHD1 in the control of global organization of polytene chromosomes. Methods: To study the action of CHD1 on global chromosome stucture, we examined the consequences of loss of CHD1 and of over-expression ATPase-dead or wild type CHD1 on polytene chromosome organisation in Drosophila larvae salivary glands. Results: In polytene chromosomes deprived of CHD1, we observed a specific bloating, blurring and shortening of the male X chromosome. Morphology of the female X chromosomes does not differ from autosomes and from the morphology of wild type chromosomes. In Chd1 null mutant males, the maternally contributed CHD1 accumulates exclusively in X-chromosome. In the wild type larvae we observed a specific enreachment of the CHD1 on the male X chromosome. Additional bands of CHD1 completely co-localize with the MSL proteins of the Dosage Compensation Complex (DCC), which associates specifically with the male X chromosome. The targeting of the CHD1 on the male X chromosome depends on the presence of a functional DCC. The loss of CHD1 results in preferential male lethality. Chd1 become essential in combination with deletion of one of two genes, encoding variant histone H3.3, His 3.3 B. An effect of Chd1 on male X-chromosome morphology is increased by the His 3.3 B deficiency. GAL4-driven ectopic expression of wild type CHD1 or its ATPase-dead form leads to a strong decompactization of the specific regions of salivary gland polytene chromosomes in euchromatin. Immunostaining with antibodies to CHD1 and elongating RNA polymerase II reveals bright staining at all sites with an altered chromatin structure. Over-expression of wild type CHD1, but not of its ATPase-dead form also results in a strong decondensation of the chromocenter, where pericentric heterochromatin fuses, and of the 4th chromosome. Decondensed heterochromatin is brightly stained with antibodies to CHD1, where CHD1 does not co-localize with RNA Pol II and where heterochromatic protein HP1and histone H1 are lost. Real – time PCR analysis have revealed that the CHD1 over-expression increases the level of replication of X-chromosome heterochromatic repeats 1.688 satellite and Stellate, however does not affect the underreplication of the heterochromatic genes in autosomes. Conclusions: Here we show that the loss or over-expression of CHD1 severely and very specifically affect the global chromatin organization of Drosophila polytene chromosomes. Our finding suggests a new link between the organization of hyperactive chromatin of the male X – chromosome and of transcriptionally silent heterochromatin. © 2019, National Academy of Sciences of Ukraine. All rights reserved.\n

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\n \n\n \n \n \n \n \n \n Isolation of Extracellular Microvesicles from Cell Culture Medium: Comparative Evaluation of Methods.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 12(2): 167-175. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Isolation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Interaction of the HIM1 gene product with helicases Srs2 (RadH) and Mph1 yeast saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Alekseeva, E.; Evstyukhina, Ò.; Peshekhonov, V.; and Korolev, V.\n\n\n \n\n\n\n Tsitologiya, 60(7): 555-557. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Interaction$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Alekseeva2018555,\r\nauthor={Alekseeva, E.A. and Evstyukhina, Ò.À. and Peshekhonov, V.T. and Korolev, V.G.},\r\ntitle={Interaction of the HIM1 gene product with helicases Srs2 (RadH) and Mph1 yeast saccharomyces cerevisiae},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={7},\r\npages={555-557},\r\ndoi={10.31116/tsitol.2018.07.13},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064719936&doi=10.31116%2ftsitol.2018.07.13&partnerID=40&md5=64eb320277936411580a125f883da59f},\r\naffiliation={B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Centre Kurchatov Institute, Gatchina, Leningrad Region, 188300, Russian Federation},\r\nabstract={We examined the interaction of the Him1 protein with the Srs2 and Mph1 helicases. These helicases are involved in the process of D-loop formation, which is the main intermediate of the error-free post-replicative repair (PRR) branch, carried out by the recombination mechanism of matrix replacement. According to our data, the HIM1 gene, the product of which is the Him1 protein, can participate in the regulation of the error-free post-replicative repair branch. PRR is the main repair system that is carried out under normal cell metabolism during replication. Disturbances in the work of PRR can lead to the appearance in humans of many inherited diseases and carcinogenesis. © 2018 Sankt Peterburg. All rights reserved.},\r\nauthor_keywords={HIM1;  Post-replicative repair;  UV-induced mutagenesis;  Yeast},\r\ncorrespondence_address1={Alekseeva, E.A.; B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Centre Kurchatov InstituteRussian Federation; email: alekseeva_ea@pnpi.nrcki.ru},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Isolation of extracellular micro-vesicles from cell culture medium: Comparative evaluation of methods.\n \n \n \n \n\n\n \n Shtam, T.; Samsonov, R.; Volnitskiy, A.; Kamyshinsky, R.; Verlov, N.; Kniazeva, M.; Korobkina, E.; Orehov, A.; Vasiliev, A.; Konevega, A.; and Malek, A.\n\n\n \n\n\n\n Biomeditsinskaya Khimiya, 64(1): 23-30. 2018.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Isolation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Shtam201823,\r\nauthor={Shtam, T.A. and Samsonov, R.A. and Volnitskiy, A.V. and Kamyshinsky, R.A. and Verlov, N.A. and Kniazeva, M.S. and Korobkina, E.A. and Orehov, A.S. and Vasiliev, A.L. and Konevega, A.L. and Malek, A.V.},\r\ntitle={Isolation of extracellular micro-vesicles from cell culture medium: Comparative evaluation of methods},\r\njournal={Biomeditsinskaya Khimiya},\r\nyear={2018},\r\nvolume={64},\r\nnumber={1},\r\npages={23-30},\r\ndoi={10.18097/PBMC20186401023},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85043459724&doi=10.18097%2fPBMC20186401023&partnerID=40&md5=b472419d6f68dab8bffc8f53af96f345},\r\naffiliation={Petersburg Nuclear Physics Institute of National Research Centre 'Kurchatov Institute', Saint-Petersburg, Gatchina, 188300, Russian Federation; 'Oncosystem' Ltd., Skolkovo, 143026, Russian Federation; N.N.Petrov National Medical Research Center of Oncology, Saint-Petersburg, 197758, Russian Federation; National Research Center 'Kurchatov Institute', Moscow, 123182, Russian Federation; Peter the Great Saint-Petersburg Polytechnic University, St. Petersburg, 195251, Russian Federation},\r\nabstract={Extracellular vesicles (EV) are secreted by cells of multicellular organisms. EV mediate specific mode of intercellular communication by "horizontal" exchange of substances and information. This phenomenon seems to have an essential biological significance and became a subject of intensive research. Biogenesis, structural and functional features of the EV is being commonly studies in in vitro condition. Several methods of EV isolation from cell culture medium are established, however selection of method might influence on obtained results. The choice of the optimal method depends usually from the amount of medium and the aims of the research while is still challenging issue. We performed a comparative analysis of four different methods of EV isolation from cell culture medium: differential ultracentrifugation, ultracentrifugation with a 30% sucrose/D2O "cushion", precipitation with plant proteins and immune-affinity capturing. EV isolated by different approaches were compared in terms of following parameters: size, concentration, morphology of EV, contamination by non-vesicular particles, content of exosomal tetraspanins on the EV surface, content of total proteins, RNA, and several glioma-associated miRNAs. Applied methods included nano-patricle tracking analysis (NTA), dynamic light scattering (DLS), cryo-electron microscopy, flow cytometry and RT-qPCR. On the base of obtained results, we developed practical recommendations that may help researchers to make a best choice of EV isolation method. © 2018 Russian Academy of Medical Sciences. All rights reserved.},\r\nauthor_keywords={Exsosomes;  Extracellular vesicles;  Immunoprecipitation;  Lectines;  Methods of isolation;  Ultracentrifugation},\r\ncorrespondence_address1={Shtam, T.A.; Petersburg Nuclear Physics Institute of National Research Centre 'Kurchatov Institute'Russian Federation; email: tatyana_shtam@mail.ru},\r\npublisher={Russian Academy of Medical Sciences},\r\nissn={23106905},\r\npubmed_id={29460831},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomeditsinskaya Khim.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2017\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Partially Assembled Nucleosome Structures at Atomic Detail.\n \n \n \n \n\n\n \n Rychkov, G.; Ilatovskiy, A.; Nazarov, I.; Shvetsov, A.; Lebedev, D.; Konev, A.; Isaev-Ivanov, V.; and Onufriev, A.\n\n\n \n\n\n\n Biophysical Journal, 112(3): 460-472. 2017.\n cited By 15\n\n\n\n
\n\n\n\n \n \n $\"Partially$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Rychkov2017460,\r\nauthor={Rychkov, G.N. and Ilatovskiy, A.V. and Nazarov, I.B. and Shvetsov, A.V. and Lebedev, D.V. and Konev, A.Y. and Isaev-Ivanov, V.V. and Onufriev, A.V.},\r\ntitle={Partially Assembled Nucleosome Structures at Atomic Detail},\r\njournal={Biophysical Journal},\r\nyear={2017},\r\nvolume={112},\r\nnumber={3},\r\npages={460-472},\r\ndoi={10.1016/j.bpj.2016.10.041},\r\nnote={cited By 15},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85009290748&doi=10.1016%2fj.bpj.2016.10.041&partnerID=40&md5=11a123be201359b0889bc6505c1b6dc0},\r\naffiliation={Division of Molecular and Radiation Biophysics, B.P. Konstantinov Petersburg Nuclear Physics Institute, National Research Center “Kurchatov Institute” Orlova Roscha, Gatchina, Russian Federation; Institute of Physics, Nanotechnology and Telecommunications, NRU Peter the Great St. Petersburg Polytechnic University, St. Petersburg, Russian Federation; Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, California, United States; Institute of Cytology, Russian Academy of Sciences, St. Petersburg, Russian Federation; Institute of Applied Mathematics and Mechanics, NRU Peter the Great St. Petersburg Polytechnic University, St. Petersburg, Russian Federation; Departments of Computer Science and Physics Virginia Tech, Blacksburg, Virginia, United States},\r\nabstract={The evidence is now overwhelming that partially assembled nucleosome states (PANS) are as important as the canonical nucleosome structure for the understanding of how accessibility to genomic DNA is regulated in cells. We use a combination of molecular dynamics simulation and atomic force microscopy to deliver, in atomic detail, structural models of three key PANS: the hexasome (H2A·H2B)·(H3·H4)2, the tetrasome (H3·H4)2, and the disome (H3·H4). Despite fluctuations of the conformation of the free DNA in these structures, regions of protected DNA in close contact with the histone core remain stable, thus establishing the basis for the understanding of the role of PANS in DNA accessibility regulation. On average, the length of protected DNA in each structure is roughly 18 basepairs per histone protein. Atomistically detailed PANS are used to explain experimental observations; specifically, we discuss interpretation of atomic force microscopy, Förster resonance energy transfer, and small-angle x-ray scattering data obtained under conditions when PANS are expected to exist. Further, we suggest an alternative interpretation of a recent genome-wide study of DNA protection in active chromatin of fruit fly, leading to a conclusion that the three PANS are present in actively transcribing regions in a substantial amount. The presence of PANS may not only be a consequence, but also a prerequisite for fast transcription in vivo. © 2017 Biophysical Society},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)obr-i 14-24-01103},\r\nfunding_details={Ministry of Education and Science of the Russian Federation8482 07.09.2012},\r\nfunding_details={Russian Science Foundation14-50-00068},\r\nfunding_details={National Institutes of HealthR01 GM099450, GM076121},\r\n}

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\n \n\n \n \n \n \n \n \n The role of remodeling complexes CHD1 and ISWI in spontaneous and UV-induced mutagenesis control in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Evstiukhina, T.; Alekseeva, E.; Fedorov, D.; Peshekhonov, V.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 53(2): 195-201. 2017.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Evstiukhina2017195,\r\nauthor={Evstiukhina, T.A. and Alekseeva, E.A. and Fedorov, D.V. and Peshekhonov, V.T. and Korolev, V.G.},\r\ntitle={The role of remodeling complexes CHD1 and ISWI in spontaneous and UV-induced mutagenesis control in yeast Saccharomyces cerevisiae},\r\njournal={Russian Journal of Genetics},\r\nyear={2017},\r\nvolume={53},\r\nnumber={2},\r\npages={195-201},\r\ndoi={10.1134/S1022795417010057},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85014863528&doi=10.1134%2fS1022795417010057&partnerID=40&md5=5110b84345e58073e0e64bc8e4955c3d},\r\naffiliation={National Research Center Kurchatov Institute, Petersburg Nuclear Physics Institute, Gatchina, Leningrad oblast, 188300, Russian Federation; Department of Biophysics, Institute of Physics, Nanotechnology, and Telecommunications, St. Petersburg State Polytechnic University, St. Petersburg, 195251, Russian Federation},\r\nabstract={Chromatin remodulators are special multiprotein machines capable of transforming the structure, constitution, and positioning of nucleosomes on DNA. Biochemical activities of remodeling complexes CHD1 and ISWI from the SWI2/SNF2 family are well established. They ensure correct positioning of nucleosomes along the genome, which is probably critical for genome stability, in particular, after action of polymerases, repair enzymes, and transcription. In this paper, we show that single mutations in genes ISW1, ISW2, and CHD1 weakly affect repair and mutagenic processes in yeast cells. At the same time, there are differences in the effect of these mutations on spontaneous mutation levels, which indicates certain specificity of action of protein complexes ISW1, ISW2, and CHD1 on expression of different genes that control repair and mutation processes in yeast. © 2017, Pleiades Publishing, Inc.},\r\nauthor_keywords={chromatin;  gene expression;  genomic stability;  repair;  transcription},\r\ncorrespondence_address1={Korolev, V.G.; National Research Center Kurchatov Institute, Petersburg Nuclear Physics InstituteRussian Federation; email: lge@omrb.pnpi.spb.ru},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Dot1 and Set2 Histone Methylases Control the Spontaneous and UV-Induced Mutagenesis Levels in the Saccharomyces cerevisiae Yeasts.\n \n \n \n \n\n\n \n Kozhina, T.; Evstiukhina, T.; Peshekhonov, V.; Chernenkov, A.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 52(3): 300-310. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Dot1$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina2016300,\r\nauthor={Kozhina, T.N. and Evstiukhina, T.A. and Peshekhonov, V.T. and Chernenkov, A.Y. and Korolev, V.G.},\r\ntitle={Dot1 and Set2 Histone Methylases Control the Spontaneous and UV-Induced Mutagenesis Levels in the Saccharomyces cerevisiae Yeasts},\r\njournal={Genetika},\r\nyear={2016},\r\nvolume={52},\r\nnumber={3},\r\npages={300-310},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85005818005&partnerID=40&md5=acc8934cdf3ad3a36db5302dd921abc5},\r\nabstract={In the Saccharomyces cerevisiae yeasts, the DOT1 gene product provides methylation of lysine 79 (K79) of hi- stone H3 and the SET2 gene product provides the methylation of lysine 36 (K36) of the same histone. We determined that the dot1 and set2 mutants suppress the UV-induced mutagenesis to an equally high degree. The dot1 mutation demonstrated statistically higher sensitivity to the low doses of MMC than the wild type strain. The analysis of the interaction between the dot1 and rad52 mutations revealed a considerable level of spontaneous cell death in the double dot1 rad52 mutant. We observed strong suppression of the gamma-in- duced mutagenesis in the set2 mutant. We determined that the dot1 and set2 mutations decrease the sponta- neous mutagenesis rate in both single and d ouble mutants. The epistatic interaction between the dot1 and set2 mutations and almost similar sensitivity of the corresponding mutants to the different types of DNA damage allow one to conclude that both genes are involved in the control of the same DNA repair pathways, the ho- mologous-recombination-based and the postreplicative DNA repair.},\r\nissn={00166758},\r\npubmed_id={27281850},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Dot1 and Set2 histone methylases control the spontaneous and UV-induced mutagenesis levels in the Saccharomyces cerevisiae yeasts.\n \n \n \n \n\n\n \n Kozhina, T.; Evstiukhina, T.; Peshekhonov, V.; Chernenkov, A.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 52(3): 263-272. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Dot1$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina2016263,\r\nauthor={Kozhina, T.N. and Evstiukhina, T.A. and Peshekhonov, V.T. and Chernenkov, A.Y. and Korolev, V.G.},\r\ntitle={Dot1 and Set2 histone methylases control the spontaneous and UV-induced mutagenesis levels in the Saccharomyces cerevisiae yeasts},\r\njournal={Russian Journal of Genetics},\r\nyear={2016},\r\nvolume={52},\r\nnumber={3},\r\npages={263-272},\r\ndoi={10.1134/S102279541602006X},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84969174531&doi=10.1134%2fS102279541602006X&partnerID=40&md5=2aabd9ced6728c91ab4022a89cf5adc0},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, St. Petersburg, Gatchina, Leningrad oblast, 188300, Russian Federation; Department of Biophysics, Institute of Physics, Nanotechnology, and Telecommunications, St. Petersburg State Polytechnic University, St. Petersburg, 195251, Russian Federation},\r\nabstract={In the Saccharomyces cerevisiae yeasts, the DOT1 gene product provides methylation of lysine 79 (K79) of histone H3 and the SET2 gene product provides the methylation of lysine 36 (K36) of the same histone. We determined that the dot1 and set2 mutants suppress the UV-induced mutagenesis to an equally high degree. The dot1 mutation demonstrated statistically higher sensitivity to the low doses of MMC than the wild type strain. The analysis of the interaction between the dot1 and rad52 mutations revealed a considerable level of spontaneous cell death in the double dot1 rad52 mutant. We observed strong suppression of the gamma-induced mutagenesis in the set2 mutant. We determined that the dot1 and set2 mutations decrease the spontaneous mutagenesis rate in both single and double mutants. The epistatic interaction between the dot1 and set2 mutations and almost similar sensitivity of the corresponding mutants to the different types of DNA damage allow one to conclude that both genes are involved in the control of the same DNA repair pathways, the homologous-recombination-based and the postreplicative DNA repair. © 2016, Pleiades Publishing, Inc.},\r\nauthor_keywords={chromatin;  DNA repair;  DOT1;  methylation;  mutagenesis;  SET2;  yeasts},\r\ncorrespondence_address1={Kozhina, T.N.; Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov InstituteRussian Federation; email: tnkozh@yandex.ru},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={10227954},\r\npubmed_id={27281850},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n THE INFLUENCE OF THE Chd1 CHROMATIN ASSEMBLY AND REMODELING FACTOR MUTATIONS ON DROSOPHILA POLYTHENE CHROMOSOME ORGANIZATION.\n \n \n \n \n\n\n \n Konev, A.; Tiutiunnik, A.; and Baranovskaya, I.\n\n\n \n\n\n\n Tsitologiia, 58(4): 281-284. 2016.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"THE$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Konev2016281,\r\nauthor={Konev, A.Y. and Tiutiunnik, A.A. and Baranovskaya, I.L.},\r\ntitle={THE INFLUENCE OF THE Chd1 CHROMATIN ASSEMBLY AND REMODELING FACTOR MUTATIONS ON DROSOPHILA POLYTHENE CHROMOSOME ORGANIZATION},\r\njournal={Tsitologiia},\r\nyear={2016},\r\nvolume={58},\r\nnumber={4},\r\npages={281-284},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85053718592&partnerID=40&md5=75edd25460d61d113333d7cd899765d3},\r\nabstract={Chromatin assembly is a fundamental process that is essential for chromosome duplication subsequent to DNA replication. In addition, histone removal and incorporation take place constantly throughout the cell cycle in the course of DNA-utilizing processes, such as transcription, damage repair or recombination. In vitro chromatin assembly requires the concerned action of histone chaperones and ATP-utilizing chromatin assembly factors. ATP-dependent chromatin assembly and remodeling factor CHD1 (Chromo-ATPase/Helicase-DNA-binding protein 1) is involved in multiple cellular processes, such as the replication independent assembly of nucleosomes containing the variant histone H3.3, regulation of transcription initiation, elongation and termination; determination of steam cell pluripotency and in cancer development. We have shown that mutations in Drosophila Chd1 gene induce a decondensation of the male X chromosome, similar to that induced by mutations in the iswi nucleosome remodeling factor. An effect of Chd1 null mutation can be increased by deficiency of one of the genes, encoding variant histone H3.3, His 3.3 B, suggesting that the role of CHD1 in the control of male X chromosome organization can be mediated by CHD1 activity in H3.3 histone deposition and exchange.},\r\nissn={00413771},\r\npubmed_id={30191695},\r\nlanguage={English},\r\nabbrev_source_title={Tsitologiia},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2015\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Histone deacetylase inhibitors cause TP53-dependent induction of p21/Waf1 in tumor cells with TP53 mutations.\n \n \n \n \n\n\n \n Kovalev, R.; Shtam, T.; Karelov, D.; Burdakov, V.; Volnitskiy, A.; Makarov, E.; and Filatova, M.\n\n\n \n\n\n\n Cell and Tissue Biology, 9(3): 191-197. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Histone$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kovalev2015191,\r\nauthor={Kovalev, R.A. and Shtam, T.A. and Karelov, D.V. and Burdakov, V.S. and Volnitskiy, A.V. and Makarov, E.M. and Filatova, M.V.},\r\ntitle={Histone deacetylase inhibitors cause TP53-dependent induction of p21/Waf1 in tumor cells with TP53 mutations},\r\njournal={Cell and Tissue Biology},\r\nyear={2015},\r\nvolume={9},\r\nnumber={3},\r\npages={191-197},\r\ndoi={10.1134/S1990519X15030086},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84934918732&doi=10.1134%2fS1990519X15030086&partnerID=40&md5=0c901448296154db7453d31299ecdd32},\r\naffiliation={Division of Molecular and Radiation Biophysics, National Research Centre “Kurchatov Institute”, Gatchina, Leningrad oblast, 188300, Russian Federation; Department of Biophysics, St. Petersburg State Polytechnical University, St. Petersburg, 194064, Russian Federation; Division of Biosciences, Brunel University, London, United Kingdom},\r\nabstract={The p21/Waf1 protein is one of the main regulators of cell cycle arrest and one of the best-known transcriptional targets of the TP53 protein. Here, we demonstrated that there is activation of expression of the p21/Waf1 gene when the cells were treated with sodium butyrate (NaBu), which is a natural histone deacetylase inhibitor, and investigated whether this phenomenon depends on the presence of a functionally active TP53 protein. For this purpose, we compared the effect of NaBu treatment of human cell lines with different TP53 mutation profiles, including wild-type TP53, single nucleotide substitutions, and the complete absence of the TP53 gene. NaBu activated the TP53 protein via hyperacetylation at the lysine residue K382, without significant changes in the level of protein expression. Western blotting showed that the addition of NaBu triggers a significant increase in the p21/Waf1 protein level in both TP53 wild-type cells and in cells with single nucleotide substitutions in the central DNA-binding core domain (DBD) of the TP53 protein. At the same time, no p21/Waf1 protein induction was observed in cells with complete deletion of the TP53 gene. However, NaBu was not able to induce p21/Waf1 production when the expression of TP53 was transiently knocked down by the p53 siRNA. Overall, our results suggest that NaBu-dependent induction of p21/Waf1 does require the presence of TP53 protein, but, unexpectedly, it can occur regardless of mutational changes in the domain responsible for the TP53 binding to DNA. One possible explanations is that NaBu increases the level of TP53 acetylation and the modified protein is able to establish a new network of protein–protein interactions or trigger conformational changes affecting the TP53-dependent transcriptional machinery even when its DNA binding ability is impaired. © 2015, Pleiades Publishing, Ltd.},\r\nauthor_keywords={HDAC inhibitors;  p21/Waf1/Cip1;  RNA interference;  sodium butyrate;  TP53;  TP53 mutations},\r\ncorrespondence_address1={Filatova, M.V.; Division of Molecular and Radiation Biophysics, National Research Centre “Kurchatov Institute”Russian Federation},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={1990519X},\r\nlanguage={English},\r\nabbrev_source_title={Cell Tissue Biol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Histone deacetylase inhibitors cause the TP53-dependent induction of p21/Waf1 in tumor cells carrying mutations in TP53.\n \n \n \n \n\n\n \n Kovalev, R.; Shtam, T.; Karelov, D.; Burdakov, V.; Volnitskiy, A.; Makarov, E.; and Filatov, M.\n\n\n \n\n\n\n Tsitologiia, 57(3): 204-211. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Histone$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kovalev2015204,\r\nauthor={Kovalev, R.A. and Shtam, T.A. and Karelov, D.V. and Burdakov, V.S. and Volnitskiy, A.V. and Makarov, E.M. and Filatov, M.V.},\r\ntitle={Histone deacetylase inhibitors cause the TP53-dependent induction of p21/Waf1 in tumor cells carrying mutations in TP53},\r\njournal={Tsitologiia},\r\nyear={2015},\r\nvolume={57},\r\nnumber={3},\r\npages={204-211},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84930790634&partnerID=40&md5=bd66a7bb8e7e0ed78b3edf4820c210f3},\r\nabstract={p21/Waf1 protein is one of the main cell cycle arrest regulators and one of the most well-known transcriptional targets of TP53 protein. Here, we demonstrated the activation of expression of the p21/Waf1 gene when the cells were treated to sodium butyrate (NaBu)--one of the natural inhibitors of deacetylase, and investigated whether this phenomenon depends on the presence of functionally active TP53 protein. We compared the effect of the NaBu treatment on the human cell line with different TP53 mutation profile, including: wild-type TP53, single nucleotide substitutions, and the complete absence of TP53 gene. NaBu activated the TP53 protein via hyper acetylation at lysine residue K382, without significant changes in the level of protein expression. Western blotting demonstrated that the addition of NaBu triggers a significant increase in the p21/Waf1 protein level in both the TP53 wild-type cells and in the cells with single nucleotide substitutions in the domain responsible for the binding of TP53 protein to DNA. At the same time, no the p21/Waf1 protein induction was observed in the cells with complete deletion of the TP53 gene. However, NaBu was not able to induce the p2 1/Waf1 production when the expression of TP53 was transiently knocked down by the p53 siRNA. Overall, our results suggest that the NaBu-dependent induction of p21/Waf1 does require the presence of TP53 protein but unexpectedly it can occur regardless of mutational changes in the domain responsible for the TP53 binding to DNA. One of the hypothetical explanations is that NaBu increases the level of TP53 acetylation, and the modified protein is able to establish a new network of protein-protein interactions or trigger some conformational changes affecting the TP53-dependent transcriptional machinery even when its DNA binding ability is impaired.},\r\nissn={00413771},\r\npubmed_id={26021170},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiia},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2014\n \n \n (5)\n \n \n

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\n \n\n \n \n \n \n \n \n [Spontaneous mutation rate changes in saccharomyces cerevisiae at combinations of hsm3 and hsm6 mutations with rad52 mutation].\n \n \n \n \n\n\n \n Chernenkov, A.; Fedorov, D.; Kosareva, A.; Kozhina, T.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 50(2): 243-245. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Spontaneous$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Chernenkov2014243,\r\nauthor={Chernenkov, A.Iu. and Fedorov, D.V. and Kosareva, A.A. and Kozhina, T.N. and Korolev, V.G.},\r\ntitle={[Spontaneous mutation rate changes in saccharomyces cerevisiae at combinations of hsm3 and hsm6 mutations with rad52 mutation]},\r\njournal={Genetika},\r\nyear={2014},\r\nvolume={50},\r\nnumber={2},\r\npages={243-245},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84925353787&partnerID=40&md5=976c5f2c25d15768d9e7bd1d00eb0c5f},\r\nabstract={Long-term storage at +4 degrees C and cultivation at +30 degrees C changes the spontaneous mutation rate of the yeast Saccharomyces cerevisiae double mutants rad52hsm3delta and rad52hsm6-1. Combinations of hsm3 and hsm6 mutations with the rad52 mutation lead to a decrease of the spontaneous mutation rate mediated by DNA repair synthesis in multiply replanted strains in comparison with the same strains investigated right after RAD52 gene decay. Combinations of hsm3 and hsm6 mutations with mutations in other genes of the RAD52 epistatic group did not provide a spontaneous mutation rate decrease.},\r\nissn={00166758},\r\npubmed_id={25711034},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Spontaneous mutation rate changes in Saccharomyces cerevisiae at combinations of hsm3 and hsm6 mutations with rad52 mutation.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 50(2): 218-220. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Spontaneous$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n [Control levels of Sin3 histone deacetylase for spontaneous and UV-induced mutagenesis in yeasts Saccharomyces cerevisiae].\n \n \n \n \n\n\n \n Lebovka, I.; Kozhina, T.; Fedorova, I.; Peshekhonov, V.; Evstiukhina, T.; Chernenkov, A.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 50(1): 5-11. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Control$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Lebovka20145,\r\nauthor={Lebovka, I.Iu. and Kozhina, T.N. and Fedorova, I.V. and Peshekhonov, V.T. and Evstiukhina, T.A. and Chernenkov, A.Iu. and Korolev, V.G.},\r\ntitle={[Control levels of Sin3 histone deacetylase for spontaneous and UV-induced mutagenesis in yeasts Saccharomyces cerevisiae]},\r\njournal={Genetika},\r\nyear={2014},\r\nvolume={50},\r\nnumber={1},\r\npages={5-11},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84925363858&partnerID=40&md5=31457bcce79426469cc933633eb217a0},\r\nabstract={SIN3 gene product operates as a repressor for a huge amount of genes in Saccharomyces cerevisiae. Sin3 protein with a mass of about 175 kDa is a member of the RPD3 protein complex with an assessed mass of greater than 2 million Da. It was previously shownthat RPD3 gene mutations influence recombination and repair processes in S. cerevisiae yeasts. We studied the impacts of the sin3 mutation on UV-light sensitivity and UV-induced mutagenesis in budding yeast cells. The deletion ofthe SIN3 gene causes weak UV-sensitivity of mutant budding cells as compared to the wild-type strain. These results show that the sin3 mutation decreases both spontaneous and UV-induced levels of levels. This fact is hypothetically related to themalfunction of ribonucleotide reductase activity regulation, which leads to a decrease in the dNTP pool and the inaccurate error-prone damage bypass postreplication repair pathway, which in turn provokes a reduction in the incidence of mutations.},\r\nissn={00166758},\r\npubmed_id={25711007},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Sin3 histone deacetylase controls level of spontaneous and UV-induced mutagenesis in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 50(1): 1-6. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Sin3$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Aberrant expression of the sox2 gene in malignant gliomas.\n \n \n \n \n\n\n \n Volnitskiy, A.; Semenova, E.; Shtam, T.; Kovalev, R.; and Filatov, M.\n\n\n \n\n\n\n Cell and Tissue Biology, 8(5): 368-373. 2014.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Aberrant$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Volnitskiy2014368,\r\nauthor={Volnitskiy, A.V. and Semenova, E.V. and Shtam, T.A. and Kovalev, R.A. and Filatov, M.V.},\r\ntitle={Aberrant expression of the sox2 gene in malignant gliomas},\r\njournal={Cell and Tissue Biology},\r\nyear={2014},\r\nvolume={8},\r\nnumber={5},\r\npages={368-373},\r\ndoi={10.1134/S1990519X14050101},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84918775524&doi=10.1134%2fS1990519X14050101&partnerID=40&md5=761056e34f65f3402cadffe380c42b4e},\r\naffiliation={Konstantinov St. Petersburg Nuclear Physics Institute, Gatchina, Russian Federation; St. Petersburg State Polytechnic University, St. Petersburg, Russian Federation},\r\nabstract={Both genetic and epigenetic changes underlie the mechanisms of tumor initiation and progression. In this study, we analyzed sox2 gene expression and its epigenetic changes in primary cultures of malignant gliomas. The sox2 expression was detected in most (74%) gliomas, but not in morphologically normal brain tissue. These facts point to relationships between the sox2 transcription activity and the process of glioma malignant transformation. It was demonstrated that association of different areas of the sox2 gene with important epigenetic markers—posttranslational modifications of H3 histone H3K4ac and H3K9met3—did not correlate with sox2 expression. However, it suggests stochastic regulation of sox2 gene expression in malignant gliomas. © 2014, Pleiades Publishing, Ltd.},\r\nauthor_keywords={aberrant gene expression;  gliomas;  posttranslational H3 histone modifications;  Sox2},\r\ncorrespondence_address1={Filatov, M.V.; Konstantinov St. Petersburg Nuclear Physics InstituteRussian Federation},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={1990519X},\r\nlanguage={English},\r\nabbrev_source_title={Cell Tissue Biol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2013\n \n \n (6)\n \n \n

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\n \n\n \n \n \n \n \n \n [Antimutagenesis of multiphytoadaptogene in yeast saccharomyces].\n \n \n \n \n\n\n \n Kurennaya, O.; Karpova, R.; Bocharova, O.; Kazeev, I.; Bocharov, E.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 49(12): 1364-1369. 2013.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Antimutagenesis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kurennaya20131364,\r\nauthor={Kurennaya, O.N. and Karpova, R.V. and Bocharova, O.A. and Kazeev, I.V. and Bocharov, E.V. and Korolev, V.G.},\r\ntitle={[Antimutagenesis of multiphytoadaptogene in yeast saccharomyces]},\r\njournal={Genetika},\r\nyear={2013},\r\nvolume={49},\r\nnumber={12},\r\npages={1364-1369},\r\ndoi={10.7868/S0016675813120059},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84922249715&doi=10.7868%2fS0016675813120059&partnerID=40&md5=0e0853497507a036e99c8acdf8e398da},\r\nabstract={Multiphytoadaptogene (MPA) consists of plant extracts components including adaptogenes. Genotoxicity analysis revealed the antimutagenic activity of MPA. MPA decreased the direct mutations frequency in ADE4-ADE8 loci induced by UV radiation and nitrous acid by 3.7 and 33 times, respectively. The lethal effect of UV radiation was inhibited when the preparation was used. MPA had no effect on replicative mutagenesis. At the same time it depressed mutagenesis caused by repair errors. The data obtained suggest the antimutagenic activity of multiphytoadaptogene is associated with postreplicative repair activation.},\r\nissn={00166758},\r\npubmed_id={25438596},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Antimutagenesis of multiphytoadaptogene in yeast Saccharomyces.\n \n \n \n \n\n\n \n Kurennaya, O.; Karpova, R.; Bocharova, O.; Kazeev, I.; Bocharov, E.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 49(12): 1190-1194. 2013.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Antimutagenesis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kurennaya20131190,\r\nauthor={Kurennaya, O.N. and Karpova, R.V. and Bocharova, O.A. and Kazeev, I.V. and Bocharov, E.V. and Korolev, V.G.},\r\ntitle={Antimutagenesis of multiphytoadaptogene in yeast Saccharomyces},\r\njournal={Russian Journal of Genetics},\r\nyear={2013},\r\nvolume={49},\r\nnumber={12},\r\npages={1190-1194},\r\ndoi={10.1134/S1022795413120053},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84890041807&doi=10.1134%2fS1022795413120053&partnerID=40&md5=47127e0f4a1bf9551494b3f2e6fa74bc},\r\naffiliation={Institute of Gene Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation; Blokhin Cancer Research Center, Russian Academy of Medical Sciences, Moscow, 115478, Russian Federation; Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow, 125315, Russian Federation; Konstantinov St. Petersburg Nuclear Physics Institute, Leningrad oblast, Gatchina, 188300, Russian Federation},\r\nabstract={Multiphytoadaptogene (MPA) consists of plant extracts components including adaptogenes. Genotoxicity analysis revealed the antimutagenic activity of MPA. MPA decreased the direct mutations frequency in ADE4-ADE8 loci induced by UV radiation and nitrous acid by 3.7 and 33 times, respectively. The lethal effect of UV radiation was inhibited when the preparation preparation MFA was used on complete medium with ethanol. MPA had no effect on replicative mutagenesis. At the same time it depressed mutagenesis caused by repair errors. The data obtained suggest the antimutagenic activity of multiphytoadaptogene is associated with postreplicative repair activation. © 2013 Pleiades Publishing, Inc.},\r\ncorrespondence_address1={Kurennaya, O. N.; Institute of Gene Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation; email: okuren@mail.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n [Structural features of chromatin organization of 3C6/C7 interband in Drosophila melanogaster polytene chromosomes].\n \n \n \n \n\n\n \n Konev, A.; Makase, A.; Pokrovskiǐ, D.; Ignat'eva, M.; Il'ina, I.; and Kotlovanova, L.\n\n\n \n\n\n\n Tsitologiia, 55(3): 198-203. 2013.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Structural$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Konev2013198,\r\nauthor={Konev, A.I. and Makase, A.A. and Pokrovskiǐ, D.K. and Ignat'eva, M.A. and Il'ina, I.A. and Kotlovanova, L.V.},\r\ntitle={[Structural features of chromatin organization of 3C6/C7 interband in Drosophila melanogaster polytene chromosomes].},\r\njournal={Tsitologiia},\r\nyear={2013},\r\nvolume={55},\r\nnumber={3},\r\npages={198-203},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84880069750&partnerID=40&md5=39dffe6477bf6fa68943f4cd8e355eb1},\r\nabstract={This article presents an analysis of the causes of chromatin decompaction of interbands in Drosophila polytene chromosomes. On the example of interband 3C6/C7 of X chromosome, we investigate the ability of different DNA segments from the region to form an interband in a new genetic environment. Site-specific FLP recombination between two transposons with FRT-sites allows introducing the DNA fragments from the inter-band 3C6/C7 into plCon(dv) transposon located in cytologically well-characterized 84F region of chromosome 3 followed by electron microscopic analysis of changes in the region, caused by insertion of the DNA fragments into the transposon. Thus, it has shown that the insertion of DNA fragment 276 bp in length from 3C6/C7 region into the plCon(dv) transposon leads to the formation of a new interband between two thin bands which are represented by material of the transposon. To date, the DNA fragment is minimal known sequence that is necessary and sufficient for interband formation. In addition, the sequence containing three tandemly repeated copies of DNA fragment 0.9 kb including a fragment of 276 bp from the interband 3C6/C7 was integrated in the transposon. The presence of additional copies of the DNA fragment did not change the morphology of the resulting interband. It was shown that sites of hypersensitivity to DNase I persist in interbands formed in the new genetic environment. The data obtained allow us to start analysis of the specific factors (proteins, DNA motifs, etc.) that determine the formation of decompacted chromatin state in sertain interband region and, as a whole, chromometric organization of interphase chromosomes in Drosophila.},\r\ncorrespondence_address1={Konev, A.I.},\r\nissn={00413771},\r\npubmed_id={23795466},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiia},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n HSM6 gene is identical to PSY4 gene in Saccharomyces cerevisiae yeasts.\n \n \n \n \n\n\n \n Fedorov, D.; Kovaltsova, S.; Evstuhina, T.; Peshekhonov, V.; Chernenkov, A.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 49(3): 286-293. 2013.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"HSM6$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Fedorov2013286,\r\nauthor={Fedorov, D.V. and Kovaltsova, S.V. and Evstuhina, T.A. and Peshekhonov, V.T. and Chernenkov, A.Y. and Korolev, V.G.},\r\ntitle={HSM6 gene is identical to PSY4 gene in Saccharomyces cerevisiae yeasts},\r\njournal={Russian Journal of Genetics},\r\nyear={2013},\r\nvolume={49},\r\nnumber={3},\r\npages={286-293},\r\ndoi={10.1134/S1022795413020063},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84875410949&doi=10.1134%2fS1022795413020063&partnerID=40&md5=2bde920adf45c6b8cbb726edf681d851},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, Gatchina, 188300, Russian Federation},\r\nabstract={Previously, we isolated mutant yeasts Saccharomyces cerevisiae with an increased rate of spontaneous mutagenesis. Here, we studied the properties of HSM6 gene, the hsm6-1 mutation of which increased the frequency of UV-induced mutagenesis and decreased the level of UV-induced mitotic crossover at the region between the centromere and ADE2 gene. HSM6 gene was mapped on the left arm of chromosome II in the region where the PSY4 gene is located. The epistatic analysis has shown that the hsm6-1 mutation represents an allele of PSY4 gene. Sequencing of hsm6-1 mutant allele has revealed a frameshift mutation, which caused the Lys218Glu substitution and the generation of a stop codon in the next position. The interactions of hsm6-1 and rad52 mutations were epistatic. Our data show that the PSY4 gene plays a key role in the regulation of cell withdrawal from checkpoint induced by DNA disturbances. © 2013 Pleiades Publishing, Ltd.},\r\ncorrespondence_address1={Fedorov, D. V.; Konstantinov Petersburg Nuclear Physics Institute, Gatchina, 188300, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n [HSM6 gene is identical to PSY4 gene in Saccharomyces cerevisiae yeasts].\n \n \n \n \n\n\n \n Fedorov, D.; Koval'tsova, S.; Evstukhina, T.; Peshekhonov, V.; Chernenkov, A.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 49(3): 328-336. 2013.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[HSM6$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Fedorov2013328,\r\nauthor={Fedorov, D.V. and Koval'tsova, S.V. and Evstukhina, T.A. and Peshekhonov, V.T. and Chernenkov, A.I. and Korolev, V.G.},\r\ntitle={[HSM6 gene is identical to PSY4 gene in Saccharomyces cerevisiae yeasts].},\r\njournal={Genetika},\r\nyear={2013},\r\nvolume={49},\r\nnumber={3},\r\npages={328-336},\r\ndoi={10.7868/S0016675813020069},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84880139857&doi=10.7868%2fS0016675813020069&partnerID=40&md5=a9b0275e625e2466d7df55659f24e151},\r\nabstract={Previously, we isolated mutant yeasts Saccharomyces cerevisiae with an increased rate of spontaneous mutagenesis. Here, we studied the properties of HSM6 gene, the hsm6-1 mutation of which increased the frequency of UV-induced mutagenesis and decreased the level of UV-induced mitotic crossover at the centromere gene region, ADE2. HSM6 gene was mapped on the left arm of chromosome 11 in the region where the PSY4 gene is located. The epistatic analysis has shown that the hsm6-1 mutation represents an allele of PSY4 gene. Sequencing of hsm6-1 mutant allele has revealed a frameshift mutation, which caused the substitution of Lys218Glu and the generation of a stop codon in the next position. The interactions of hsm6-1 and rad52 mutations were epistatic. Our data show that the PSY4 gene plays a key role in the regulation of cell withdrawal from checkpoint induced by DNA disturbances.},\r\ncorrespondence_address1={Fedorov, D.V.},\r\nissn={00166758},\r\npubmed_id={23755532},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Antioxidant prophylaxis of radiation stress.\n \n \n \n \n\n\n \n Koltover, V.; Korolev, V.; and Kutlakhmedov, Y.\n\n\n \n\n\n\n Nova Science Publishers, Inc., 2013.\n cited By 6\n\n\n\n
\n\n\n\n \n \n $\"Antioxidant$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@BOOK{Koltover2013117,\r\nauthor={Koltover, V.K. and Korolev, V.G. and Kutlakhmedov, Y.A.},\r\ntitle={Antioxidant prophylaxis of radiation stress},\r\njournal={Ionizing Radiation: Applications, Sources and Biological Effects},\r\nyear={2013},\r\npages={117-127},\r\nnote={cited By 6},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84895206110&partnerID=40&md5=6b812cc9f59dedb6eb3a5240329d7419},\r\naffiliation={Institute of Problems of Chemical Physics, Russian Academy of Sciences, Chernogolovka, Moscow Region, Russian Federation; Petersburg Institute of Nuclear Physics, Gatchina, Leningrad Region, Russian Federation; Institute of Cell Biology and Genetic Engineering, National Academy of Sciences of Ukraine, Kyiv, Ukraine},\r\nabstract={Once atomic power engineering has become a part of our everyday lives, the special precautions should be taken to reduce harmful effects of radiation for specialists in atomic industry as well as for people in the contaminated territories after atomic accidents. To defend the people in case of chronic radiation, novel radiation protectors, which would be non-toxic and suited to long-time applications as nutrients, are required. The water-soluble antioxidants based on alkyl-substituted hydroxypyridines have been long used with success in medical practice. In the experiments with yeast cells, S. cerevisiae, we have revealed that 3-hydroxy-6-methyl-2-ethylpyridine essentially improves post-radiation recovery and raises survivability of the cells after γ-irradiation (60Co, 800 Gy). Of special interest, can be some magnetic isotopes. Among three stable isotopes of magnesium, 24Mg, 25Mg, and 26Mg with natural abundance approximately 79, 10, and 11 %, only 25Mg has the nuclear spin (I = 5/2) and, hence, the nuclear magnetic field, while 24Mg and 26Mg have no nuclear spin (I = 0) and magnetic field. We have revealed that the rate constant of post-radiation recovery of cells after short-wave UV irradiation was twice higher for the cells enriched with magnetic 25Mg, when compared to the cells enriched with the nonmagnetic isotope. Thus, the stable magnetic isotope of magnesium, as well as the non-toxic antioxidants, hold promises for creating novel radio-protectors suitable as nutrients for use at chronic radiation. [Supported by Russian Foundation for Basic Research, grant 10-03-01203a]. © 2012 Nova Science Publishers, Inc. All rights reserved.},\r\nauthor_keywords={Antioxidant prophylaxis;  Radiation protectors;  Radiation stress;  Reliability;  Robustness;  Stable magnetic isotopes},\r\ncorrespondence_address1={Koltover, V.K.; Institute of Problems of Chemical Physics, Russian Academy of Sciences, Chernogolovka, Moscow Region, Russian Federation; email: koltover@icp.ac.ru},\r\npublisher={Nova Science Publishers, Inc.},\r\nisbn={9781622573431},\r\nlanguage={English},\r\nabbrev_source_title={Ioniz. Radiat.: Appl., Sources and Biol. Eff.},\r\ndocument_type={Book Chapter},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n [RAD18 gene product of yeast Saccharomyces cerevisiae controls mutagenesis induced by hydrogen peroxide].\n \n \n \n \n\n\n \n Kozhina, T.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 48(4): 551-555. 2012.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[RAD18$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina2012551,\r\nauthor={Kozhina, T.N. and Korolev, V.G.},\r\ntitle={[RAD18 gene product of yeast Saccharomyces cerevisiae controls mutagenesis induced by hydrogen peroxide].},\r\njournal={Genetika},\r\nyear={2012},\r\nvolume={48},\r\nnumber={4},\r\npages={551-555},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84864514014&partnerID=40&md5=c7068af448c2b9a2ecb4cf6ebe0a8943},\r\nabstract={Within eukaryotes, tolerance to DNA damage is determined primarily by the repair pathway controlled by the members of the RAD6 epistasis group. Genetic studies on a yeast Saccharomyces cerevisiae model showed that the initial stage of postreplication repair (PRR), i.e., initiation of replication through DNA damage, is controlled by Rad6-Rad18 ubiquitin-conjugating enzyme complex. Mutants of these genes are highly sensitive to various genotoxic agents and reduce the level of induced mutagenesis. In this case, the efficiency of mutagenesis suppression depends on the type of damage. In this study we showed that DNA damage induced by hydrogen peroxide at the same mutagen doses causes significantly more mutations and lethal events in the rad18 mutant cells compared to control wild-type cells.},\r\ncorrespondence_address1={Kozhina, T.N.},\r\nissn={00166758},\r\npubmed_id={22730775},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n RAD18 gene product of yeast Saccharomyces cerevisiae controls mutagenesis induced by hydrogen peroxide.\n \n \n \n \n\n\n \n Kozhina, T.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 48(4): 463-467. 2012.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"RAD18$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina2012463,\r\nauthor={Kozhina, T.N. and Korolev, V.G.},\r\ntitle={RAD18 gene product of yeast Saccharomyces cerevisiae controls mutagenesis induced by hydrogen peroxide},\r\njournal={Russian Journal of Genetics},\r\nyear={2012},\r\nvolume={48},\r\nnumber={4},\r\npages={463-467},\r\ndoi={10.1134/S1022795412010127},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84860367786&doi=10.1134%2fS1022795412010127&partnerID=40&md5=a3b74f6c8614a8a6d6af280ef0cd0735},\r\naffiliation={Konstantinov Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningradskaya oblast 188300, Russian Federation},\r\nabstract={Within eukaryotes, tolerance to DNA damage is determined primarily by the repair pathway controlled by the members of the RAD6 epistasis group. Genetic studies on a yeast Saccharomyces cerevisiae model showed that the initial stage of postreplication repair (PRR), i. e., initiation of replication through DNA damage, is controlled by Rad6-Rad18 ubiquitin-conjugating enzyme complex. Mutants of these genes are highly sensitive to various genotoxic agents and reduce the level of induced mutagenesis. In this case, the efficiency of mutagenesis suppression depends on the type of damage. In this study we showed that DNA damage induced by hydrogen peroxide at the same mutagen doses causes significantly more mutations and lethal events in the rad18 mutant cells compared to control wild-type cells. © 2012 Pleiades Publishing, Ltd.},\r\n}

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\n \n\n \n \n \n \n \n \n Identification and characterization of ToRC, a novel ISWI-containing ATP-dependent chromatin assembly complex.\n \n \n \n \n\n\n \n Emelyanov, A.; Vershilova, E.; Ignatyeva, M.; Pokrovsky, D.; Lu, X.; Konev, A.; and Fyodorov, D.\n\n\n \n\n\n\n Genes and Development, 26(6): 603-614. 2012.\n cited By 15\n\n\n\n
\n\n\n\n \n \n $\"Identification$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Emelyanov2012603,\r\nauthor={Emelyanov, A.V. and Vershilova, E. and Ignatyeva, M.A. and Pokrovsky, D.K. and Lu, X. and Konev, A.Y. and Fyodorov, D.V.},\r\ntitle={Identification and characterization of ToRC, a novel ISWI-containing ATP-dependent chromatin assembly complex},\r\njournal={Genes and Development},\r\nyear={2012},\r\nvolume={26},\r\nnumber={6},\r\npages={603-614},\r\ndoi={10.1101/gad.180604.111},\r\nnote={cited By 15},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84858328711&doi=10.1101%2fgad.180604.111&partnerID=40&md5=b624425b6cd96c424ad5e3ef19235982},\r\naffiliation={Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States; Molecular and Radiation Biophysics Department, St. Petersburg Nuclear Physics Institute, Gatchina 188300, Russian Federation},\r\nabstract={SNF2-like motor proteins, such as ISWI, cooperate with histone chaperones in the assembly and remodeling of chromatin. Here we describe a novel, evolutionarily conserved, ISWI-containing complex termed ToRC (Toutatiscontaining chromatin remodeling complex). ToRC comprises ISWI, Toutatis/TIP5 (TTF-I-interacting protein 5), and the transcriptional corepressor CtBP (C-terminal-binding protein). ToRC facilitates ATP-dependent nucleosome assembly in vitro. All three subunits are required for its maximal biochemical activity. The toutatis gene exhibits strong synthetic lethal interactions with CtBP. Thus, ToRC mediates, at least in part, biological activities of CtBP and Toutatis. ToRC subunits colocalize in euchromatic arms of polytene chromosomes. Furthermore, nuclear localization and precise distribution of ToRC in chromosomes are dependent on CtBP. ToRC is involved in CtBP-mediated regulation of transcription by RNA polymerase II in vivo. For instance, both Toutatis and CtBP are required for repression of genes of a proneural gene cluster, achaete-scute complex (AS-C), in Drosophila larvae. Intriguingly, native C-terminally truncated Toutatis isoforms do not associate with CtBP and localize predominantly to the nucleolus. Thus, Toutatis forms two alternative complexes that have differential distribution and can participate in distinct aspects of nuclear DNA metabolism. © 2012 by Cold Spring Harbor Laboratory Press.},\r\nauthor_keywords={Ac-sc complex (AS-C);  Chromatin assembly and remodeling;  CtBP;  ISWI;  Nucleolus;  TIP5;  Toutatis},\r\ncorrespondence_address1={Fyodorov, D. V.; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States; email: dmitry.fyodorov@einstein.yu.edu},\r\nissn={08909369},\r\ncoden={GEDEE},\r\npubmed_id={22426536},\r\nlanguage={English},\r\nabbrev_source_title={Genes Dev.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n [Interaction of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae].\n \n \n \n \n\n\n \n Chernenkov, A.; Fedorov, D.; Gracheva, L.; Evstukhina, T.; Koval'tsova, S.; Peshekhonov, V.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 48(3): 333-339. 2012.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Interaction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Chernenkov2012333,\r\nauthor={Chernenkov, A.I. and Fedorov, D.V. and Gracheva, L.M. and Evstukhina, T.A. and Koval'tsova, S.V. and Peshekhonov, V.T. and Fedorova, I. and Korolev, V.},\r\ntitle={[Interaction of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae].},\r\njournal={Genetika},\r\nyear={2012},\r\nvolume={48},\r\nnumber={3},\r\npages={333-339},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84864380159&partnerID=40&md5=372482e5e392263858f26547a037c103},\r\nabstract={It was assumed previously that the mutator phenotype of the hms3 mutant was determined by processes taking place in the D-loop. As a next step, genetic analysis was performed to study the interactions between the hsm3 mutation and mutations of the genes that control the initial steps of the D-loop formation. The mutations of the MMS4 and XRS2 genes, which initiate the double-strand break formation and subsequent repair, were shown to completely block HSM3-dependent UV-induced mutagenesis. Mutations of the RAD51, RAD52, and RAD54 genes, which are also involved in the D-loop formation, only slightly decreased the level of UV-induced mutagenesis in the hsm3 mutant. Similar results were observed for the interaction of hsm3 with the mph1 mutation, which stabilizes the D-loop. In contrast, the shu1 mutation, which destabilizes the D-loop structure, led to an extremely high level of UV-induced mutagenesis and displayed epistatic interactions with the hsm3 mutation. The results made it possible to assume that the hsm3 mutation destabilizes the D-loop, which is a key substrate of both Rad5- and Rad52-dependent postreplicative repair pathways.},\r\ncorrespondence_address1={Chernenkov, A.I.},\r\nissn={00166758},\r\npubmed_id={22679780},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Interactions of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Chernenkov, A.; Fedorov, D.; Gracheva, L.; Evstuhina, T.; Kovaltsova, S.; Peshekhonov, V.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 48(3): 284-290. 2012.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Interactions$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Chernenkov2012284,\r\nauthor={Chernenkov, A.Y. and Fedorov, D.V. and Gracheva, L.M. and Evstuhina, T.A. and Kovaltsova, S.V. and Peshekhonov, V.T. and Fedorova, I.V. and Korolev, V.G.},\r\ntitle={Interactions of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae},\r\njournal={Russian Journal of Genetics},\r\nyear={2012},\r\nvolume={48},\r\nnumber={3},\r\npages={284-290},\r\ndoi={10.1134/S1022795412020056},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84858958855&doi=10.1134%2fS1022795412020056&partnerID=40&md5=48650634e167655dc9b933c51d891e27},\r\naffiliation={Konstantinov St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad oblast 188350, Russian Federation},\r\nabstract={It was assumed previously that the mutator phenotype of the hms3 mutant was determined by processes taking place in the D-loop. As a next step, genetic analysis was performed to study the interactions between the hsm3 mutation and mutations of the genes that control the initial steps of the D-loop formation. The mutations of the MMS4 and XRS2 genes, which initiate the double-strand break formation and subsequent repair, were shown to completely block HSM3-dependent UV-induced mutagenesis. Mutations of the RAD51, RAD52, and RAD54 genes, which are also involved in the D-loop formation, only slightly decreased the level of UV-induced mutagenesis in the hsm3 mutant. Similar results were observed for the interaction of hsm3 with the mph1 mutation, which stabilizes the D-loop. In contrast, the shu1 mutation, which destabilizes the D-loop structure, led to an extremely high level of UV-induced mutagenesis and displayed epistatic interactions with the hsm3 mutation. The results made it possible to assume that the hsm3 mutation destabilizes the D-loop, which is a key substrate of both Rad5- and Rad52-dependent postreplicative repair pathways. © 2012 Pleiades Publishing, Ltd.},\r\ncorrespondence_address1={Chernenkov, A. Y.; Konstantinov St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad oblast 188350, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n [Interaction of gene HSM3 with genes of the epistatic RAD6 group in yeast Saccharomyces cerevisiae].\n \n \n \n \n\n\n \n Chernenkov, A.; Gracheva, L.; Evstiukhina, T.; Koval'tsova, S.; Peshekhonov, V.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 48(2): 160-167. 2012.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Interaction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Chernenkov2012160,\r\nauthor={Chernenkov, A.I. and Gracheva, L.M. and Evstiukhina, T.A. and Koval'tsova, S.V. and Peshekhonov, V.T. and Fedorova, I.V. and Korolev, V.G.},\r\ntitle={[Interaction of gene HSM3 with genes of the epistatic RAD6 group in yeast Saccharomyces cerevisiae].},\r\njournal={Genetika},\r\nyear={2012},\r\nvolume={48},\r\nnumber={2},\r\npages={160-167},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84861512455&partnerID=40&md5=beab3ef727b73d14980b17f9fdb17490},\r\nabstract={In eukaryotes, damage tolerance of matrix DNA is mainly determined by the repair pathway under the control of the RAD6 epistatic group of genes. T this pathway is also a main source of mutations generated by mutagenic factors. The results of our recent studies show that gene HSM3 participating in the control of adaptive mutagenesis increases the frequency of mutations induced by different mutagens. Mutations rad18, rev3, and mms2 controlling various stages of the RAD6 pathway are epistatic with mutation hsm3 that decreases UV-induced mutagenesis to the level typical for single radiation-sensitive mutants. The level of mutagenesis in the double mutant srs2 hsm3 was lower than in both single mutants. Note that a decrease in the level of mutagenesis relative to the single mutant srs2 depends on the mismatch repair, since this level in the triple mutant srs2 hsm3 pms 1 corresponds to that in the single mutant srs2. These data show that the mutator phenotype hsm3 is probably determined by processes occurring in a D loop. In a number of current works, the protein Hsm3 was shown to participate in the assembly of the proteasome complex S26. The assembly of proteasomes is governed by the N-terminal domain. Our results demonstrated that the Hsm3 protein contains at least two domains; the N-terminal part of the domain is responsible for the proteasome assembly, whereas the C-terminal portion of the protein is responsible for mutagenesis.},\r\ncorrespondence_address1={Chernenkov, A.I.},\r\nissn={00166758},\r\npubmed_id={22567994},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n

\n \n\n \n \n \n \n \n \n Interaction of gene HSM3 with genes of the Epistatic RAD6 group in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Chernenkov, A.; Gracheva, L.; Evstyukhina, T.; Koval'tsova, S.; Peshekhonov, V.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 48(2): 139-145. 2012.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Interaction$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Chernenkov2012139,\r\nauthor={Chernenkov, A.Y. and Gracheva, L.M. and Evstyukhina, T.A. and Koval'tsova, S.V. and Peshekhonov, V.T. and Fedorova, I.V. and Korolev, V.G.},\r\ntitle={Interaction of gene HSM3 with genes of the Epistatic RAD6 group in yeast Saccharomyces cerevisiae},\r\njournal={Russian Journal of Genetics},\r\nyear={2012},\r\nvolume={48},\r\nnumber={2},\r\npages={139-145},\r\ndoi={10.1134/S102279541201005X},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84857481115&doi=10.1134%2fS102279541201005X&partnerID=40&md5=d90f99774b3050acbc56536613555cdf},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Leningradskaya oblast, Gatchina 188300, Russian Federation},\r\nabstract={In eukaryotes, damage tolerance of matrix DNA is mainly determined by the repair pathway under the control of the RAD6 epistatic group of genes. This pathway is also a main source of mutations generated by mutagenic factors. The results of our recent studies show that gene HSM3 participating in the control of adaptive mutagenesis increases the frequency of mutations induced by different mutagens. Mutations rad18, rev3, and mms2 controlling various stages of the RAD6 pathway are epistatic with mutation hsm3 that decreases UV-induced mutagenesis to the level typical for single radiation-sensitive mutants. The level of mutagenesis in the double mutant srs2 hsm3 was lower than in both single mutants. Note that a decrease in the level of mutagenesis relative to the single mutant srs2 depends on the mismatch repair, since this level in the triple mutant srs2 hsm3 pms1 corresponds to that in the single mutant srs2. These data show that the mutator phenotype hsm3 is probably determined by processes occurring in a D loop. In a number of current works, the protein Hsm3 was shown to participate in the assembly of the proteasome complex S26. The assembly of proteasomes is governed by the N-terminal domain. Our results demonstrated that the Hsm3 protein contains at least two domains; the N-terminal part of the domain is responsible for the proteasome assembly, whereas the C-terminal portion of the protein is responsible for mutagenesis. © 2012 Pleiades Publishing, Ltd.},\r\ncorrespondence_address1={Chernenkov, A. Y.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Leningradskaya oblast, Gatchina 188300, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2011\n \n \n (5)\n \n \n

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\n \n\n \n \n \n \n \n \n Study of the epigenetic regulation of transpositions of nonautonomous P-elements in Drosophila at different temperatures.\n \n \n \n \n\n\n \n Ilina, Y.; Varentsova, E.; Kotlovanova, L.; Konev, A.; and Khromykh, Y.\n\n\n \n\n\n\n Russian Journal of Genetics: Applied Research, 1(2): 155-159. 2011.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Study$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Ilina2011155,\r\nauthor={Ilina, Y.A. and Varentsova, E.R. and Kotlovanova, L.V. and Konev, A.Y. and Khromykh, Y.M.},\r\ntitle={Study of the epigenetic regulation of transpositions of nonautonomous P-elements in Drosophila at different temperatures},\r\njournal={Russian Journal of Genetics: Applied Research},\r\nyear={2011},\r\nvolume={1},\r\nnumber={2},\r\npages={155-159},\r\ndoi={10.1134/S207905971102002X},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84864775965&doi=10.1134%2fS207905971102002X&partnerID=40&md5=bc015ad45877f7399cdf6ca9f44c10c0},\r\naffiliation={Konstantinov St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nabstract={In a system of Drosophila P-element activation at 25 and 18°C, we observed an increase in the gene conversion frequency among the offspring of parents containing nonautonomous P-elements and a chromosome with the rad201G1 mutation in the genome. A similar increase in conversion events in this system was shown in experiments with the mutation mei41D5. In both cases, inheritance of the increased conversion was also observed among offspring not carrying the rad201G1 or mei41D5 mutations. © 2011 Pleiades Publishing, Ltd.},\r\nauthor_keywords={epigenetic regulation;  gene conversion;  P-elements;  recombination;  repair},\r\ncorrespondence_address1={Ilina, Y. A.; Konstantinov St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nissn={20790597},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Genet. Appl. Res.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n [Gene RAD31 is identical to gene MEC1 of yeast Saccharomyces cerevisiae].\n \n \n \n \n\n\n \n Kozhina, T.; Kozhin, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 47(5): 610-614. 2011.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"[Gene$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Kozhina2011610,\r\nauthor={Kozhina, T.N. and Kozhin, S.A. and Korolev, V.G.},\r\ntitle={[Gene RAD31 is identical to gene MEC1 of yeast Saccharomyces cerevisiae].},\r\njournal={Genetika},\r\nyear={2011},\r\nvolume={47},\r\nnumber={5},\r\npages={610-614},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-80052584179&partnerID=40&md5=868c68b4d2d1f5ea6bb23204e65dde76},\r\nabstract={The earlier identified gene RAD31 was mapped on the right arm of chromosome II in the region of gene MEC1 localization. Epistatic analysis demonstrated that the rad31 mutation is an allele of the MEC1 gene, which allows further designation of the rad31 mutation as mec1-212. Mutation mec1-212, similar to deletion alleles of this gene, causes sensitivity to hydroxyurea, disturbs the check-point function, and suppresses UV-induced mutagenesis. However, this mutation significantly increases the frequency of spontaneous canavanine-resistance mutations induced by disturbances in correcting errors of DNA replication and repair, which distinguishes it from all identified alleles of gene MEC1.},\r\ncorrespondence_address1={Kozhina, T.N.},\r\nissn={00166758},\r\npubmed_id={21786666},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Gene RAD31 is identical to gene MEC1 of yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Kozhina, T.; Kozhin, S.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 47(5): 533-537. 2011.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Gene$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Kozhina2011533,\r\nauthor={Kozhina, T.N. and Kozhin, S.A. and Korolev, V.G.},\r\ntitle={Gene RAD31 is identical to gene MEC1 of yeast Saccharomyces cerevisiae},\r\njournal={Russian Journal of Genetics},\r\nyear={2011},\r\nvolume={47},\r\nnumber={5},\r\npages={533-537},\r\ndoi={10.1134/S1022795411020104},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-79956093086&doi=10.1134%2fS1022795411020104&partnerID=40&md5=d0bb620a7d59e8bbe3b04b9c03acb6fa},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, St. Petersburg 188300, Russian Federation},\r\nabstract={The earlier identified gene RAD31 was mapped on the right arm of chromosome II in the region of gene MEC1 localization. Epistatic analysis demonstrated that the rad31 mutation is an allele of the MEC1 gene, which allows further designation of the rad31 mutation as mec1-212. Mutation mec1-212, similar to deletion alleles of this gene, causes sensitivity to hydroxyurea, disturbs the check-point function, and suppresses UV-induced mutagenesis. However, this mutation significantly increases the frequency of spontaneous canavanine-resistance mutations induced by disturbances in correcting errors of DNA replication and repair, which distinguishes it from all identified alleles of gene MEC1. © 2011 Pleiades Publishing, Ltd.},\r\n}

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\n \n\n \n \n \n \n \n \n [Chromatin and DNA damage repair].\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Genetika, 47(4): 449-459. 2011.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Chromatin$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev2011449,\r\nauthor={Korolev, V.G.},\r\ntitle={[Chromatin and DNA damage repair].},\r\njournal={Genetika},\r\nyear={2011},\r\nvolume={47},\r\nnumber={4},\r\npages={449-459},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-80052040247&partnerID=40&md5=ba1490357b3b39b1b6475e4eef8cf277},\r\nabstract={In eukaryotic cells, inheritance of both exact DNA sequence and its arrangement into the chromatin is critical for maintaining stability of the genome. Various DNA lesions induced by endogenous and exogenous factors make this maintenance problematic. To understand completely how cells resolve this problem the knowledge on the nature of these lesions, their detection, and repair within the chromatin environment should be integrated. Understanding of these processes is complicated by multiple types of DNA lesions and repair pathways, as well as the intricate organization of the chromatin. Recent advances in all these directions help to get insight on the repair regulation of DNA within the chromatin at the molecular and cellular level.},\r\ncorrespondence_address1={Korolev, V.G.},\r\nissn={00166758},\r\npubmed_id={21675233},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n Chromatin and DNA damage repair.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 47(4): 394-403. 2011.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Chromatin$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev2011394,\r\nauthor={Korolev, V.G.},\r\ntitle={Chromatin and DNA damage repair},\r\njournal={Russian Journal of Genetics},\r\nyear={2011},\r\nvolume={47},\r\nnumber={4},\r\npages={394-403},\r\ndoi={10.1134/S1022795411030082},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-79955032795&doi=10.1134%2fS1022795411030082&partnerID=40&md5=9991bb0cd49c092f99dee3ac4ccbf985},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Gatchina, Leningrad region 188300, Russian Federation},\r\nabstract={In eukaryotic cells, inheritance of both exact DNA sequence and its arrangement into the chromatin is critical for maintaining stability of the genome. Various DNA lesions induced by endogenous and exogenous factors make this maintanance problematic. To understand completely how cells resolve this problem the knowledge on the nature of these lesions, their detection, and repair within the chromatin environment should be integrated. Understanding of these processes is complicated by multiple types of DNA lesions and repair pathways, as well as the intricate organization of the chromatin. Recent advances in all these directions help to get insight on the repair regulation of DNA within the chromatin at the molecular and cellular level. © 2011 Pleiades Publishing, Ltd.},\r\nfunding_details={07 04 00256},\r\n}

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\n \n 2010\n \n \n (7)\n \n \n

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\n \n\n \n \n \n \n \n \n IXR1 and HMO1 genes jointly control the level of spontaneous mutagenesis in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 46(6): 659-665. 2010.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"IXR1$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Genetic analysis of the Hsm3 protein domain structure in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 46(6): 652-658. 2010.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n IXR1 and HMO1 genes jointly control the level of spontaneous mutagenesis in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Fedorov, D.; Koval'tsova, S.; Peshekhonov, V.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 46(6): 750-757. 2010.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"IXR1$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Fedorov2010750,\r\nauthor={Fedorov, D.V. and Koval'tsova, S.V. and Peshekhonov, V.T. and Korolev, V.G.},\r\ntitle={IXR1 and HMO1 genes jointly control the level of spontaneous mutagenesis in yeast Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={2010},\r\nvolume={46},\r\nnumber={6},\r\npages={750-757},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77957253654&partnerID=40&md5=569f478364dce0548b9357bed3a785fe},\r\nabstract={The yeast genes IXR1 and HMO1 encode proteins belonging to the family of chromatin nonhistone proteins, which are able to recognize and bind to irregular DNA structures. The full deletion of gene IXR1 leads to an increase in cell resistance to the lethal action of UV light, gamma-rays, and MMS, increases spontaneous mutagenesis and significantlly decreases the level of UV-induced mutations. It was earlier demonstrated in our works that the hmo 1 mutation renders cells sensitive to the lethal action of cisplatin and virtually does not affect the sensitivity to UV light. Characteristically, the rates of spontaneous and UV-induced mutagenesis in the mutant are increased. Epistatic analysis of the double mutation hmo 1 ixr1 demonstrated that the interaction of these genes in relation to the lethal effect of cisplatin and UV light, as well as UV-induced mutagenesis, is additive. This suggests that the products of genes HMO1 and IXR1 participate in different repair pathways. The ixr1 mutation significantly increases the rate of spontaneous mutagenesis mediated by replication errors, whereas mutation hmo 1 increases the rate of repair mutagenesis. In wild-type cells, the level of spontaneous mutagenesis was nearly one order of magnitude lower than that obtained in cells of the double mutant. Consequently, the combined activity of the Hmo 1 and the Ixr1 proteins provides efficient correction of both repair and replication errors.},\r\ncorrespondence_address1={Fedorov, D.V.},\r\nissn={00166758},\r\npubmed_id={20734765},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic analysis of the Hsm3 protein domain structure in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Chernenkov, A.; Ivanova, S.; Koval'tsova, S.; Gracheva, L.; Peshekhonov, V.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 46(6): 742-749. 2010.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Chernenkov2010742,\r\nauthor={Chernenkov, A.I. and Ivanova, S.V. and Koval'tsova, S.V. and Gracheva, L.M. and Peshekhonov, V.T. and Fedorova, I.V. and Korolev, V.G.},\r\ntitle={Genetic analysis of the Hsm3 protein domain structure in yeast Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={2010},\r\nvolume={46},\r\nnumber={6},\r\npages={742-749},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77957269025&partnerID=40&md5=12a833f84410fb081ca08b4bb29e57a3},\r\nabstract={Gene HSM3 encodes the Hsm3 protein involved in the minor branch in the system responsible for the correction of mismatched bases in DNA structure and controls replicative and reparative spontaneous mutagenesis in yeast Saccharomyces cerevisiae. Spontaneous and UV-induced mutagenesis was studied in three mutant alleles of gene HSM3, and repair effectivity of artificial heteroduplexes was assessed in DNA molecule. The resuts of these studies allowed establishment of the protein domain structure of protein Hsm3 and functions of each domain: the N-terminal domain is responsible for binding to mispaired bases, and the C-terminal domain ensures the interaction with other proteins involved in the system of mismatched base correction.},\r\ncorrespondence_address1={Chernenkov, A.I.},\r\nissn={00166758},\r\npubmed_id={20734764},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Protein complex of Drosophila ATRX/XNP and HP1a is required for the formation of pericentric beta-heterochromatin in vivo.\n \n \n \n \n\n\n \n Emelyanov, A.; Konev, A.; Vershilova, E.; and Fyodorov, D.\n\n\n \n\n\n\n Journal of Biological Chemistry, 285(20): 15027-15037. 2010.\n cited By 26\n\n\n\n
\n\n\n\n \n \n $\"Protein$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Emelyanov201015027,\r\nauthor={Emelyanov, A.V. and Konev, A.Y. and Vershilova, E. and Fyodorov, D.V.},\r\ntitle={Protein complex of Drosophila ATRX/XNP and HP1a is required for the formation of pericentric beta-heterochromatin in vivo},\r\njournal={Journal of Biological Chemistry},\r\nyear={2010},\r\nvolume={285},\r\nnumber={20},\r\npages={15027-15037},\r\ndoi={10.1074/jbc.M109.064790},\r\nnote={cited By 26},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77952025217&doi=10.1074%2fjbc.M109.064790&partnerID=40&md5=072881d4c833e1c2a8a211596e48e508},\r\naffiliation={Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States; Sydney Kimmel Foundation for Cancer Research, Australia},\r\nabstract={ATRX belongs to the family of SWI2/SNF2-like ATP-dependent nucleosome remodeling molecular motor proteins. Mutations of the human ATRX gene result in a severe genetic disorder termed X-linked α-thalassemia mental retardation (ATR-X) syndrome. Here we perform biochemical and genetic analyses of the Drosophila melanogaster ortholog of ATRX. The loss of function allele of the Drosophila ATRX/XNP gene is semilethal. Drosophila ATRX is expressed throughout development in two isoforms, p185 and p125. ATRX185 and ATRX125 form distinct multisubunit complexes in fly embryo. The ATRX185 complex comprises p185 and heterochromatin protein HP1a. Consistently, ATRX185 but not ATRX125 is highly concentrated in pericentric beta-heterochromatin of the X chromosome in larval cells. HP1a strongly stimulates biochemical activities of ATRX185 in vitro. Conversely, ATRX185 is required for HP1a deposition in pericentric beta-heterochromatin of the X chromosome. The loss of function allele of the ATRX/XNP gene and mutant allele that does not express p185 are strong suppressors of position effect variegation. These results provide evidence for essential biological functions of Drosophila ATRX in vivo and establish ATRX as a major determinant of pericentric beta-heterochromatin identity. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.},\r\ncorrespondence_address1={Fyodorov, D. V.1300 Morris Park Ave., Bronx, NY 10461, United States; email: dfyodoro@aecom.yu.edu},\r\nissn={00219258},\r\ncoden={JBCHA},\r\npubmed_id={20154359},\r\nlanguage={English},\r\nabbrev_source_title={J. Biol. Chem.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The role of the Rdh54 protein in regulation of DNA repair in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 46(2): 170-177. 2010.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n The Rdh54 protein role in regulation of DNA repair in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Latypov, V.; Kozhina, T.; Kozhin, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 46(2): 194-202. 2010.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Latypov2010194,\r\nauthor={Latypov, V.F. and Kozhina, T.N. and Kozhin, S.A. and Korolev, V.G.},\r\ntitle={The Rdh54 protein role in regulation of DNA repair in yeast Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={2010},\r\nvolume={46},\r\nnumber={2},\r\npages={194-202},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77951630209&partnerID=40&md5=cc1dbe352138c5a7605610ee03af65be},\r\nabstract={In this work, we present the evidences of the involvement of Rdh54 in coordination of DNA repair by several pathways. Previously, we isolated rdh54-29 point mutation demonstrating unique properties different from the full deletion of RDH54 gene. Epistatic interaction between rdh54-29 and apn1delta mutations discloses the function of Rdh54p in the process of base excision repair. However, rdh54-29 mutant exhibits sensitivity to many DNA damaging agents including UV light, methylmethanesulphonate and nitrous acid. Such pleiotrophic effect of rdh54-29 mutation may indicate the role of Rdh54p in the regulation of different DNA repair systems. To check this hypothesis, we estimated the effect of rdh54-29 mutation on recombination and mutagenesis. The data confirm the involvement of Rdh54p in coordination of different DNA repair systems including mutagenic and recombinagenic pathways as well as nucleotide excision repair. Rdh54p presumably operates via chromatin remodulation at the site of damage rendering DNA accessible to the DNA repair enzymes.},\r\ncorrespondence_address1={Latypov, V.F.},\r\nissn={00166758},\r\npubmed_id={20297653},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2009\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n Linker histone H1 is essential for Drosophila development, the establishment of pericentric heterochromatin, and a normal polytene chromosome structure.\n \n \n \n \n\n\n \n Lu, X.; Wontakal, S.; Emelyanov, A.; Morcillo, P.; Konev, A.; Fyodorov, D.; and Skoultchi, A.\n\n\n \n\n\n\n Genes and Development, 23(4): 452-465. 2009.\n cited By 58\n\n\n\n
\n\n\n\n \n \n $\"Linker$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Lu2009452,\r\nauthor={Lu, X. and Wontakal, S.N. and Emelyanov, A.V. and Morcillo, P. and Konev, A.Y. and Fyodorov, D.V. and Skoultchi, A.I.},\r\ntitle={Linker histone H1 is essential for Drosophila development, the establishment of pericentric heterochromatin, and a normal polytene chromosome structure},\r\njournal={Genes and Development},\r\nyear={2009},\r\nvolume={23},\r\nnumber={4},\r\npages={452-465},\r\ndoi={10.1101/gad.1749309},\r\nnote={cited By 58},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-61449102557&doi=10.1101%2fgad.1749309&partnerID=40&md5=00282a7b8edf4b5af4211a934ba62d8d},\r\naffiliation={Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States; Departamento de Genética, Universidad de Valencia, Doctor Moliner 50, E46100 Burjassot, Valencia, Spain; Molecular and Radiation Biophysics Department, St. Petersburgh Nuclear Physics Institute, Gatchina 188300, Russian Federation},\r\nabstract={We generated mutant alleles of Drosophila melanogaster in which expression of the linker histone H1 can be down-regulated over a wide range by RNAi. When the H1 protein level is reduced to -20% of the level in wild-type larvae, lethality occurs in the late larval -pupal stages of development. Here we show that H1 has an important function in gene regulation within or near heterochromatin. It is a strong dominant suppressor of position effect variegation (PEV). Similar to other suppressors of PEV, H1 is simultaneously involved in both the repression of euchromatic genes brought to the vicinity of pericentric heterochromatin and the activation of heterochromatic genes that depend on their pericentric localization for maximal transcriptional activity. Studies of H1-depleted salivary gland polytene chromosomes show that H1 participates in several fundamental aspects of chromosome structure and function. First, H1 is required for heterochromatin structural integrity and the deposition or maintenance of major pericentric heterochromatin-associated histone marks, including H3K9Me2 and H4K20Me2. Second, H1 also plays an unexpected role in the alignment of endoreplicated sister chromatids. Finally, H1 is essential for organization of pericentric regions of all polytene chromosomes into a single chromocenter. Thus, linker histone H1 is essential in Drosophila and plays a fundamental role in the architecture and activity of chromosomes in vivo.},\r\nauthor_keywords={Chromocenter;  Heterochromatin;  Histone methylation;  Linker histone H1;  Polytene chromosomes;  Position effect variegation},\r\ncorrespondence_address1={Fyodorov, D. V.; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States; email: dfyodoro@aecom.yu.edu},\r\nissn={08909369},\r\ncoden={GEDEE},\r\npubmed_id={19196654},\r\nlanguage={English},\r\nabbrev_source_title={Genes Dev.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2008\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n The geptrong pharmaceutical product increases efficiency of postreplication repair of permutation intermediates in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Kovaltsova, S.; Fedorova, I.; Gracheva, L.; Mashistov, S.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 44(11): 1272-1279. 2008.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kovaltsova20081272,\r\nauthor={Kovaltsova, S.V. and Fedorova, I.V. and Gracheva, L.M. and Mashistov, S.A. and Korolev, V.G.},\r\ntitle={The geptrong pharmaceutical product increases efficiency of postreplication repair of permutation intermediates in yeast Saccharomyces cerevisiae},\r\njournal={Russian Journal of Genetics},\r\nyear={2008},\r\nvolume={44},\r\nnumber={11},\r\npages={1272-1279},\r\ndoi={10.1134/S1022795408110045},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-60349098057&doi=10.1134%2fS1022795408110045&partnerID=40&md5=cb4c6a4414783df2b53703ebd5a72657},\r\naffiliation={St. Petersburg Konstantinov Nuclear Physics Institute, Russian Academy of Sciences, Leningrad oblast, Gatchina 188300, Russian Federation; Novopharma Company, Tashkent 100084, Uzbekistan},\r\nabstract={Geptrong is a medication from pure defermentated honey. In medical practice, it is used as hepatoprotector. Genotoxicity analysis revealed antimutagenic activity of the preparation. The spontaneous mutation rate at the ADE4-ADE8 and CAN1 loci was several times lower in case that the yeast cells were plated on the geptrong-containing medium, and the mutation rate was scored using the method of ordered plating. If spontaneous mutation rate was measured by means of the fluctuation method of median, no antimutagenic activity was detected. Geptrong had no effect on the yeast cell survival. At the same time, it substantially decreased the frequency of direct mutations at the ADE4-ADE8 locus, induced by UV-and gamma-radiation, and ethylmetansulfonate. The effect of the geptrong antimutagenic activity on the level of UV-induced mutagenesis in the yeast strains defective for the repair systems rad2, rad51, rad54, rad59, msh2, and hsm3 was examined. Antimutagenic activity was detected in the wild type, as well as in the rad2, rad54, rad59, and hsm3 strains, while rad51, pms1, and msh2 mutants lacked this activity. Based on these data, it is suggested that antimutagenic effect of geptrong is associated with activated repair of mismatches, appeared during the postreplicative recombination repair. © 2008 Pleiades Publishing, Ltd.},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)04-04-480179},\r\n}

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\n \n\n \n \n \n \n \n \n Genetic analysis reveals different roles of Schizosaccharomyces pombe sfr1/dds20 in meiotic and mitotic DNA recombination and repair.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Current Genetics, 54(4): 197-211. 2008.\n cited By 8\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n 2007\n \n \n (4)\n \n \n

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\n \n\n \n \n \n \n \n \n CHD1 motor protein is required for deposition of histone variant H3.3 into chromatin in vivo.\n \n \n \n \n\n\n \n Konev, A.; Tribus, M.; Sung, Y.; Podhraski, V.; Chin, Y.; Emelyanov, A.; Vershilova, E.; Pirrotta, V.; Kadonaga, J.; Lusser, A.; and Fyodorov, D.\n\n\n \n\n\n\n Science, 317(5841): 1087-1090. 2007.\n cited By 174\n\n\n\n
\n\n\n\n \n \n $\"CHD1$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Konev20071087,\r\nauthor={Konev, A.Y. and Tribus, M. and Sung, Y.P. and Podhraski, V. and Chin, Y.L. and Emelyanov, A.V. and Vershilova, E. and Pirrotta, V. and Kadonaga, J.T. and Lusser, A. and Fyodorov, D.V.},\r\ntitle={CHD1 motor protein is required for deposition of histone variant H3.3 into chromatin in vivo},\r\njournal={Science},\r\nyear={2007},\r\nvolume={317},\r\nnumber={5841},\r\npages={1087-1090},\r\ndoi={10.1126/science.1145339},\r\nnote={cited By 174},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-34548272156&doi=10.1126%2fscience.1145339&partnerID=40&md5=5ce007d56f27b9cfe0f3ddfcbe4295ee},\r\naffiliation={Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, United States; Division of Molecular Biology, Biocenter, Innsbruck Medical University, Fritz-Pregl Strasse 3, A-6020 Innsbruck, Austria; Department of Molecular Biology and Biochemistry, Rutgers University, 604 Allison Road, Piscataway, NJ 08854, United States; Section of Molecular Biology, University of California at San Diego, San Diego, CA 92093, United States; Stem Cell and Developmental Biology Group, Genome Institute of Singapore, 60 Biopolis Street, S138672, Singapore, Singapore},\r\nabstract={The organization of chromatin affects all aspects of nuclear DNA metabolism in eukaryotes. H3.3 is an evolutionarily conserved histone variant and a key substrate for replication-independent chromatin assembly. Elimination of chromatin remodeling factor CHD1 in Drosophila embryos abolishes incorporation of H3.3 into the male pronucleus, renders the paternal genome unable to participate in zygotic mitoses, and leads to the development of haploid embryos. Furthermore, CHD1, but not ISWI, interacts with HIRA in cytoplasmic extracts. Our findings establish CHD1 as a major factor in replacement histone metabolism in the nucleus and reveal a critical role for CHD1 in the earliest developmental instances of genome-scale, replication-independent nucleosome assembly. Furthermore, our results point to the general requirement of adenosine triphosphate (ATP) - utilizing motor proteins for histone deposition in vivo.},\r\ncorrespondence_address1={Lusser, A.; Division of Molecular Biology, Biocenter, Innsbruck Medical University, Fritz-Pregl Strasse 3, A-6020 Innsbruck, Austria; email: alexandra.lusser@i-med.ac.at},\r\nissn={00368075},\r\ncoden={SCIEA},\r\npubmed_id={17717186},\r\nlanguage={English},\r\nabbrev_source_title={Science},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Molecular mechanisms of double strand break repair in eukaryotes.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Radiatsionnaia biologiia, radioecologiia / Rossiǐskaia akademiia nauk, 47(4): 389-401. 2007.\n cited By 6\n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev2007389,\r\nauthor={Korolev, V.G.},\r\ntitle={Molecular mechanisms of double strand break repair in eukaryotes},\r\njournal={Radiatsionnaia biologiia, radioecologiia / Rossiǐskaia akademiia nauk},\r\nyear={2007},\r\nvolume={47},\r\nnumber={4},\r\npages={389-401},\r\nnote={cited By 6},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-38449114743&partnerID=40&md5=9d08c843f98ec74e32c9fd2f8c08f943},\r\nabstract={Genome stability is of primary importance for the survival and for the proper functioning of all organisms. Double strand breaks (DSBs) arise spontaneously during growth, or can be created by external insults. In response to even a single DSB, organisms must trigger series of events to promote repair of the DNA damage in order to survive and restore chromosome integrity. In doing so, cells must regulate a fine balance between potentially competing DSB repair pathways. Much of what we know today on the mechanisms of repair in eukaryotes come from studies carried out in budding yeast. In this review, the main attention is focused on exciting new work eminating from yeast research that provides fresh insights into the DSB repair process.},\r\ncorrespondence_address1={Korolev, V.G.},\r\nissn={08698031},\r\npubmed_id={17953425},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiats Biol Radioecol},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres.\n \n \n \n \n\n\n \n Frydrychova, R.; Biessmann, H.; Konev, A.; Golubovsky, M.; Johnson, J.; Archer, T.; and Mason, J.\n\n\n \n\n\n\n Molecular and Cellular Biology, 27(13): 4991-5001. 2007.\n cited By 10\n\n\n\n
\n\n\n\n \n \n $\"Transcriptional$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Frydrychova20074991,\r\nauthor={Frydrychova, R.C. and Biessmann, H. and Konev, A.Y. and Golubovsky, M.D. and Johnson, J. and Archer, T.K. and Mason, J.M.},\r\ntitle={Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres},\r\njournal={Molecular and Cellular Biology},\r\nyear={2007},\r\nvolume={27},\r\nnumber={13},\r\npages={4991-5001},\r\ndoi={10.1128/MCB.00515-07},\r\nnote={cited By 10},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-34347334554&doi=10.1128%2fMCB.00515-07&partnerID=40&md5=2e1e3d8862cdbce7a3bfeeea7866e8f2},\r\naffiliation={Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, United States; Developmental Biology Center, University of California, Irvine, CA 92697, United States; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, United States; Laboratory of Molecular Genetics, D3-01, National Institute of Environmental Health Sciences, 111 T. W. Alexander Drive, Res. Triangle Park, NC 27709-2233, United States; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, United States; Center for Demographic Studies, Duke University, Durham, NC, United States},\r\nabstract={Drosophila melanogaster telomeres have two DNA domains: a terminal array of retrotransposons and a subterminal repetitive telomere-associated sequence (TAS), a source of telomere position effect (TPE). We reported previously that deletion of the 2L TAS array leads to dominant suppression of TPE by stimulating in trans expression of a telomeric transgene. Here, we compared the transcript activities of a w transgene inserted between the retrotransposon and TAS arrays at the 2L telomere in genotypes with different lengths of the 2L TAS. In contrast to individuals bearing a wild-type 2L homologue, flies with a TAS deficiency showed a significant increase in the level of telomeric w transcript during development, especially in pupae. Moreover, we identified a read-through w transcript initiated from a retrotransposon promoter in the terminal array. Read-through transcript levels also significantly increased with the presence of a 2L TAS deficiency in trans, indicating a stimulating force of the TAS deficiency on retrotransposon promoter activity. The read-through transcript contributes to total w transcript, although most w transcript originates at the w promoter. While silencing of transgenes in nonhomologous telomeres is suppressed by 2L TAS deficiencies, suggesting a global effect, the overall level of HeT-A transcripts is not increased under similar conditions.},\r\ncorrespondence_address1={Mason, J.M.; Laboratory of Molecular Genetics, D3-01, National Institute of Environmental Health Sciences, 111 T. W. Alexander Drive, Res. Triangle Park, NC 27709-2233, United States; email: masonj@niehs.nih.gov},\r\nissn={02707306},\r\ncoden={MCEBD},\r\npubmed_id={17470550},\r\nlanguage={English},\r\nabbrev_source_title={Mol. Cell. Biol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Repair of cisplatin-DNA adducts in mutants for genes controlling spontaneous and induced mutagenesis in Saccharomyces cerevisiae yeast.\n \n \n \n \n\n\n \n Kovaltsova, S.; Chernenkov, A.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 43(1): 84-87. 2007.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Repair$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kovaltsova200784,\r\nauthor={Kovaltsova, S.V. and Chernenkov, A.Yu. and Korolev, V.G.},\r\ntitle={Repair of cisplatin-DNA adducts in mutants for genes controlling spontaneous and induced mutagenesis in Saccharomyces cerevisiae yeast},\r\njournal={Russian Journal of Genetics},\r\nyear={2007},\r\nvolume={43},\r\nnumber={1},\r\npages={84-87},\r\ndoi={10.1134/S1022795407010139},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-33846700528&doi=10.1134%2fS1022795407010139&partnerID=40&md5=70eae7b128bdf05c45d43ab8f93f161a},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, Leningrad oblast' 188300, Russian Federation},\r\nabstract={Sensitivity to the lethal action of the anticancer substance cisplatin was studied in the yeast mutants him1, hsm2, hsm3, and hsm6, deficient for repair of spontaneous and induced mutations. The him1 and hsm3 mutants were as resistant to the agent under study as the wild-type strain. The survival of the double mutant rad2 hsm3 was higher than that of the single mutant rad2. The hsm2 and hsm6 mutants were more cisplatin-sensitive than the wild type. Cisplatin was shown to have high mutagenic and recombinogenic effects on yeast cells. © 2007 Pleiades Publishing, Inc.},\r\ncorrespondence_address1={Kovaltsova, S.V.; Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, Leningrad oblast' 188300, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2006\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n Transferase and hydrolytic activities of the laminarinase from rhodothermus marinus and its M133A, M133C, and M133W mutants.\n \n \n \n \n\n\n \n Neustroev, K.; Golubev, A.; Sinnott, M.; Borriss, R.; Krah, M.; Brumer III, H.; Eneyskaya, E.; Shishlyannikov, S.; Shabalin, K.; Peshechonov, V.; Korolev, V.; and Kulminskaya, A.\n\n\n \n\n\n\n Glycoconjugate Journal, 23(7-8): 501-511. 2006.\n cited By 9\n\n\n\n
\n\n\n\n \n \n $\"Transferase$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Neustroev2006501,\r\nauthor={Neustroev, K.N. and Golubev, A.M. and Sinnott, M.L. and Borriss, R. and Krah, M. and Brumer III, H. and Eneyskaya, E.V. and Shishlyannikov, S. and Shabalin, K.A. and Peshechonov, V.T. and Korolev, V.G. and Kulminskaya, A.A.},\r\ntitle={Transferase and hydrolytic activities of the laminarinase from rhodothermus marinus and its M133A, M133C, and M133W mutants},\r\njournal={Glycoconjugate Journal},\r\nyear={2006},\r\nvolume={23},\r\nnumber={7-8},\r\npages={501-511},\r\ndoi={10.1007/s10719-006-6733-0},\r\nnote={cited By 9},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-33749165434&doi=10.1007%2fs10719-006-6733-0&partnerID=40&md5=40a9fe7a331bd7dd7076485066cc694e},\r\naffiliation={Petersburg Nuclear Physics Institute, Russian Academy of Science, Molecular and Radiation Biology Division, Gatchina 188300, Russian Federation; Department of Chemical and Biological Sciences, University of Huddersfield, Queensgate, Huddersfield HD1 3DH, United Kingdom; AG Bakteriengenetik, Institut fur Biologie, Humboldt Universitt Berlin, Chausseestrasse 117, Berlin D-10115, Germany; Department of Biotechnology, Royal Institute of Technology (KTH), AlbaNova University Centre, Stockholm S-106 91, Sweden},\r\nabstract={Comparative studies of the transglycosylation and hydrolytic activities have been performed on the Rhodothermus marinus β-1,3-glucanase (laminarinase) and its M133A, M133C, and M133W mutants. The M133C mutant demonstrated near 20% greater rate of transglycosylation activity in comparison with the M133A and M133W mutants that was measured by NMR quantitation of nascent β(1-4) and β(1-6) linkages. To obtain kinetic probes for the wild-type enzyme and Met-133 mutants, p-nitrophenyl β-laminarin oligosaccharides of degree of polymerisation 2-8 were synthesized enzymatically. Catalytic efficiency values, k cat/K m, of the laminarinase catalysed hydrolysis of these oligosaccharides suggested possibility of four negative and at least three positive binding subsites in the active site. Comparison of action patterns of the wild-type and M133C mutant in the hydrolysis of the p-nitrophenyl-β-D-oligosac- charides indicated that the increased transglycosylation activity of the M133C mutant did not result from altered subsite affinities. The stereospecificity of the transglycosylation reaction also was unchanged in all mutants; the major transglycosylation products in hydrolysis of p-nitrophenyl laminaribioside were β-glucopyranosyl-β-1,3-D-glucopy- ranosyl-β-1,3-D-glucopyranose and β-glucopyranosyl-β-1, 3-D-glucopyranosyl-β-1,3-D- glucpyranosyl-β-1,3-D- glucopyranoxside. © 2006 Springer Science + Business Media, LLC.},\r\nauthor_keywords={Laminarinase;  p-nitrophenyl β-laminarin oligosaccharides;  Rhodothermus marinus;  Transglycosylation},\r\nfunding_details={Russian Academy of Sciences03-04-48756},\r\n}

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\n \n 2005\n \n \n (7)\n \n \n

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\n \n\n \n \n \n \n \n \n Base excision repair: AP endonucleases and DNA polymerases.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Genetika, 41(10): 1301-1309. 2005.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Base$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev20051301,\r\nauthor={Korolev, V.G.},\r\ntitle={Base excision repair: AP endonucleases and DNA polymerases},\r\njournal={Genetika},\r\nyear={2005},\r\nvolume={41},\r\nnumber={10},\r\npages={1301-1309},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-33644800486&partnerID=40&md5=2e63b1c7cd618dc6fb27f769045d7f81},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, Leningrad oblast, 188300, Russian Federation},\r\nabstract={The DNA base lesions in living cells occur permanently and with high frequency as a result of the action of exogenous and endogenous factors. The main mechanism providing removal of such lesions is base excision repair.},\r\ncorrespondence_address1={Korolev, V.G.; Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, Leningrad oblast, 188300, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={16316001},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Base excision repair of DNA: Glycosylases.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Genetika, 41(6): 725-735. 2005.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Base$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev2005725,\r\nauthor={Korolev, V.G.},\r\ntitle={Base excision repair of DNA: Glycosylases},\r\njournal={Genetika},\r\nyear={2005},\r\nvolume={41},\r\nnumber={6},\r\npages={725-735},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-26944470397&partnerID=40&md5=fbacc73a6af80d7f97e4c266314de821},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad Oblast, 188300, Russian Federation},\r\nabstract={The review considers the role of base excision repair in maintaining the constancy of genetic information in the cell. The genetic control and biochemical mechanism are described for the first stage of base excision repair, which is catalyzed by specific enzymes, DNA glycosylases.},\r\ncorrespondence_address1={Korolev, V.G.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad Oblast, 188300, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={16080596},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The dds20+ gene controls a novel Rad51Sp-dependent pathway of recombinational repair in Schizosaccharomyces pombe.\n \n \n \n \n\n\n \n Salakhova, A.; Savchenko, G.; Khasanov, F.; Chepurnaya, O.; Korolev, V.; and Bashkirov, V.\n\n\n \n\n\n\n Genetika, 41(6): 736-745. 2005.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Salakhova2005736,\r\nauthor={Salakhova, A.F. and Savchenko, G.V. and Khasanov, F.K. and Chepurnaya, O.V. and Korolev, V.G. and Bashkirov, V.I.},\r\ntitle={The dds20+ gene controls a novel Rad51Sp-dependent pathway of recombinational repair in Schizosaccharomyces pombe},\r\njournal={Genetika},\r\nyear={2005},\r\nvolume={41},\r\nnumber={6},\r\npages={736-745},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-26944502386&partnerID=40&md5=591dbca9aba46d5f6fc6eeb400460529},\r\naffiliation={Institute of Gene Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad Oblast, 188300, Russian Federation},\r\nabstract={Repair of DNA double-strand break (DSB) is an evolutionary conserved Rad51-mediated mechanism. In yeasts, Rad51 paralogs, Saccharomyces cerevisiae Rad55-Rad57 and Schizosaccharomyces pombe Rhp55-Rhp57 are mediators of the nucleoprotein Rad51 filament formation. As shown in this work, a novel RAD51Sp-dependent pathway of DSB repair acts in S. pombe parallel to the pathway mediated by Rad51 paralogs. A new gene dds20+ that controls this pathway was identified. The overexpression of dds20+ partially suppresses defects of mutant rhp55Δ in DNA repair. Cells of dds20Δ manifest hypersensitivity to a variety of genotoxins. Epistatic analysis revealed that dds20+ is a gene of the recombinational repair group. The role of Dds20 in repair of spontaneous damages occurring in the process of replication and mating-type switching remains unclear. The results obtained suggest that Dds20 has functions beyond the mitotic S phase. The Dds20 protein physically interacts with Rhp51(Rad51Sp). Dds20 is assumed to operate at early recombinational stages and to play a specific role in the Rad51 protein filament assembly differing from that of Rad51 paralogs.},\r\ncorrespondence_address1={Salakhova, A.F.; Institute of Gene Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={16080597},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n HIM1, a new yeast Saccharomyces cerevisiae gene playing a role in control of spontaneous and induced mutagenesis.\n \n \n \n \n\n\n \n Kelberg, E.; Kovaltsova, S.; Alekseev, S.; Fedorova, I.; Gracheva, L.; Evstukhina, T.; and Korolev, V.\n\n\n \n\n\n\n Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 578(1-2): 64-78. 2005.\n cited By 8\n\n\n\n
\n\n\n\n \n \n $\"HIM1,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kelberg200564,\r\nauthor={Kelberg, E.P. and Kovaltsova, S.V. and Alekseev, S.Yu. and Fedorova, I.V. and Gracheva, L.M. and Evstukhina, T.A. and Korolev, V.G.},\r\ntitle={HIM1, a new yeast Saccharomyces cerevisiae gene playing a role in control of spontaneous and induced mutagenesis},\r\njournal={Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis},\r\nyear={2005},\r\nvolume={578},\r\nnumber={1-2},\r\npages={64-78},\r\ndoi={10.1016/j.mrfmmm.2005.03.003},\r\nnote={cited By 8},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-25844510752&doi=10.1016%2fj.mrfmmm.2005.03.003&partnerID=40&md5=ab29b612a8226b3e7ce593a617cc1bb2},\r\naffiliation={Laboratory of Eukaryote Genetics, Division of Molecular and Radiation Biophysics, Petersburg Nuclear Physics Institute, 188350 Orlova Roscha, Gatchina, Leningrad District, Russian Federation},\r\nabstract={We have identified a new Saccharomyces cerevisiae gene, HIM1, mapped on the right arm of the chromosome IV (ORF YDR317w), mutations in which led to an increase in spontaneous mutation rate and elevated the frequencies of mutations, induced by UV-light, nitrous acid, ethylmethane sulfonate and methylmethane sulfonate. At the same time, him1 mutation did not result in the increase of the sensitivity to the lethal action of these DNA-damaging agents. We tested the induced mutagenesis in double mutants carrying him1 mutation and mutations in other repair genes: apn1, blocking base excision repair; rad2, rev3, and rad54, blocking three principal DNA repair pathways; pms1, blocking mismatch repair; hsm2 and hsm3 mutations, which lead to a mutator effect. Epistatic analysis showed a synergistic interaction of him1 with pms1, apn1, and rad2 mutations, and epistasis with the rev3, the rad54, the hsm2, and the hsm3. To elucidate the role of the HIM1 in control of spontaneous mutagenesis, we checked the repair of DNA mispaired bases in the him1 mutant and discovered that it was not altered in comparison to the wild-type strain. In our opinion, our results suggest that HIM1 gene participates in the control of processing of mutational intermediates appearing during error-prone bypass of DNA damage. © 2005 Elsevier B.V. All rights reserved.},\r\nauthor_keywords={DNA repair;  him1 mutant;  Mutagenesis;  Yeast},\r\n}

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\n \n\n \n \n \n \n \n \n Base excision repair: AP endonucleases and DNA polymerases.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 41(10): 1063-1070. 2005.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Base$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev20051063,\r\nauthor={Korolev, V.G.},\r\ntitle={Base excision repair: AP endonucleases and DNA polymerases},\r\njournal={Russian Journal of Genetics},\r\nyear={2005},\r\nvolume={41},\r\nnumber={10},\r\npages={1063-1070},\r\ndoi={10.1007/s11177-005-0201-y},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-27844448826&doi=10.1007%2fs11177-005-0201-y&partnerID=40&md5=c86b1a37ff766f3ab4519c1a2db5f043},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, Leningrad Oblast, 188300, Russian Federation},\r\nabstract={The DNA base lesions in living cells occur permanently and with high frequency as a result of the action of exogenous and endogenous factors. The main mechanism providing removal of such lesions is base excision repair. © 2005 Pleiades Publishing, Inc.},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)04-04-48179},\r\n}

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\n \n\n \n \n \n \n \n \n Base excision repair of DNA: Glycosylases.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 41(6): 583-592. 2005.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Base$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev2005583,\r\nauthor={Korolev, V.G.},\r\ntitle={Base excision repair of DNA: Glycosylases},\r\njournal={Russian Journal of Genetics},\r\nyear={2005},\r\nvolume={41},\r\nnumber={6},\r\npages={583-592},\r\ndoi={10.1007/s11177-005-0131-8},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-23744443374&doi=10.1007%2fs11177-005-0131-8&partnerID=40&md5=0d7f0fc708243044ad730c08d4a088fa},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad Oblast, 188300, Russian Federation},\r\nabstract={The review considers the role of base excision repair in maintaining the constancy of genetic information in the cell. The genetic control and biochemical mechanism are described for the first stage of base excision repair, which is catalyzed by specific enzymes, DNA glycosylases. © 2005 Pleiades Publishing, Inc.},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)04-04-48179},\r\n}

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\n \n\n \n \n \n \n \n \n The dds20 + gene controls a novel Rad51Sp-dependent pathway of recombinational repair in Schizosaccharomyces pombe.\n \n \n \n \n\n\n \n Salakhova, A.; Savchenko, G.; Khasanov, F.; Chepurnaya, O.; Korolev, V.; and Bashkirov, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 41(6): 593-601. 2005.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Salakhova2005593,\r\nauthor={Salakhova, A.F. and Savchenko, G.V. and Khasanov, F.K. and Chepurnaya, O.V. and Korolev, V.G. and Bashkirov, V.I.},\r\ntitle={The dds20 + gene controls a novel Rad51Sp-dependent pathway of recombinational repair in Schizosaccharomyces pombe},\r\njournal={Russian Journal of Genetics},\r\nyear={2005},\r\nvolume={41},\r\nnumber={6},\r\npages={593-601},\r\ndoi={10.1007/s11177-005-0132-7},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-23744438816&doi=10.1007%2fs11177-005-0132-7&partnerID=40&md5=6cef6f44490a2453edc4631744109f42},\r\naffiliation={Institute of Gene Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad Oblast, 188300, Russian Federation},\r\nabstract={Repair of DNA double-strand break (DSB) is an evolutionary conserved Rad51-mediated mechanism. In yeasts, Rad51 paralogs, Saccharomyces cerevisiae Rad55-Rad57 and Schizosaccharomyces pombe Rhp55-Rhp57 are mediators of the nucleoprotein Rad51 filament formation. As shown in this work, a novel Rad51Sp-dependent pathway of DSB repair acts in S. pombe parallel to the pathway mediated by Rad51 paralogs. A new gene dds20 + that controls this pathway was identified. The overexpression of dds20 + partially suppresses defects of mutant rhp55Δ in DNA repair. Cells of dds20Δ manifest hypersensitivity to a variety of genotoxins. Epistatic analysis revealed that dds20 + is a gene of the recombinational repair group. The role of Dds20 in repair of spontaneous damages occurring in the process of replication and mating-type switching remains unclear. The results obtained suggest that Dds20 has functions beyond the mitotic S phase. The Dds20 protein physically interacts with Rhp51(Rad51Sp). Dds20 is assumed to operate at early recombinational stages and to play a specific role in the Rad51 protein filament assembly differing from that of Rad51 paralogs. © 2005 Pleiades Publishing, Inc.},\r\ncorrespondence_address1={Salakhova, A.F.; Institute of Gene Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2004\n \n \n (3)\n \n \n

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\n \n\n \n \n \n \n \n \n A deficiency screen for dominant suppressors of telomeric silencing in Drosophila.\n \n \n \n \n\n\n \n Mason, J.; Ransom, J.; and Konev, A.\n\n\n \n\n\n\n Genetics, 168(3): 1353-1370. 2004.\n cited By 20\n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Mason20041353,\r\nauthor={Mason, J.M. and Ransom, J. and Konev, A.Y.},\r\ntitle={A deficiency screen for dominant suppressors of telomeric silencing in Drosophila},\r\njournal={Genetics},\r\nyear={2004},\r\nvolume={168},\r\nnumber={3},\r\npages={1353-1370},\r\ndoi={10.1534/genetics.104.030676},\r\nnote={cited By 20},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-10844286385&doi=10.1534%2fgenetics.104.030676&partnerID=40&md5=c05af6d95e1a2bba1d2f4dba8c67aa4a},\r\naffiliation={Laboratory of Molecular Genetics, Natl. Inst. of Environ. Hlth. Sci., Res. Triangle Park, NC 27709-2233, United States; Laboratory of Molecular Genetics, Natl. Inst. of Environ. Hlth. Sci., P.O. Box 12233, Res. Triangle Park, NC 27709-2233, United States; Department of Molecular Biology, Univ. of TX Southwestern Med. Center, Dallas, TX 75390, United States; Postgenomics, San Diego, CA 92121, United States},\r\nabstract={Heterochromatin is a specialized chromatin structure in chromosomal regions associated with repeated DNA sequences and low concentrations of genes. Formation of heterochromatin is determined in large part by enzymes that modify histones and structural proteins that bind to these modified histones in a cooperative fashion. In Drosophila, mutations in genes that encode heterochromatic proteins are often dominant and increase expression of genes placed into heterochromatic positions. To find components of telomeric heterochromatin in Drosophila, we screened a collection of autosomal deficiencies for dominant suppressors of silencing of a transgene at the telomere of chromosome 2L. While many deficiency chromosomes are associated with dominant suppressors, in the cases tested on chromosome 2 the suppressor mapped to the 2L telomere, rather than the deficiency. We infer that background effects may hamper the search for genes that play a role in telomeric heterochromatin formation and that either very few genes participate in this pathway or mutations in these genes are not dominant suppressors of telomeric position effect. The data also suggest that the 2L telomere region plays a major role in telomeric silencing.},\r\ncorrespondence_address1={Mason, J.M.; Laboratory of Molecular Genetics, Natl. Inst. of Environ. Hlth. Sci., P.O. Box 12233, Res. Triangle Park, NC 27709-2233, United States; email: masonj@niehs.nih.gov},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={15579690},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Identification and characterization of the rlp1+, the novel Rad51 paralog in the fission yeast Schizosaccharomyces pombe.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n DNA Repair, 3(10): 1363-1374. 2004.\n cited By 16\n\n\n\n
\n\n\n\n \n \n $\"Identification$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Requirement of HSM3 gene for spontaneous mutagenesis in Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Fedorova, I.; Kovaltzova, S.; Gracheva, L.; Evstuhina, T.; and Korolev, V.\n\n\n \n\n\n\n Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 554(1-2): 67-75. 2004.\n cited By 11\n\n\n\n
\n\n\n\n \n \n $\"Requirement$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Fedorova200467,\r\nauthor={Fedorova, I.V. and Kovaltzova, S.V. and Gracheva, L.M. and Evstuhina, T.A. and Korolev, V.G.},\r\ntitle={Requirement of HSM3 gene for spontaneous mutagenesis in Saccharomyces cerevisiae},\r\njournal={Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis},\r\nyear={2004},\r\nvolume={554},\r\nnumber={1-2},\r\npages={67-75},\r\ndoi={10.1016/j.mrfmmm.2004.03.003},\r\nnote={cited By 11},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-4344603733&doi=10.1016%2fj.mrfmmm.2004.03.003&partnerID=40&md5=d6efefe34f7fee4e39b1899ac465c612},\r\naffiliation={Laboratory of Eucaryote Genetics, Div. of Molec. and Radiat. Biophys., Petersburg Nucl. Phys. Inst., R., Gatchina, Russian Federation},\r\nabstract={In this work, we studied the influence of hsm3 mutation on spontaneous mutagenesis in actively and slowly dividing cells. We demonstrated that the spontaneous mutation rates in the hsm3 mutant and the wild type strain were similar in actively dividing cells. However, during 15-day cultivation of both strains we observed higher accumulation of mutants in the hsm3 strain compared with those in the wild type cells. Effect of accumulation of spontaneous mutants was observed in slowly dividing cells in the rad1, rad2, rad14, rad54, and pms1, but it was absent in the rev3, pol2 and pol3 mutants. Combinations of the hsm3 mutation with the pol3-01, pol2-04 and pms1Δ mutations decreased significantly the level of spontaneous mutagenesis in rapidly growing cells. The hsm3 mutation suppressed synthetic lethality in the hsm3 pol3-01 pms1 triple mutant and dramatically increased the spontaneous mutation rate in comparison with double mutant. The introduction of the hsm3 mutation in NER-mutants led to considerably increasing of the spontaneous mutation level. The double hsm3 rev3, hsm3 rad54 and hsm3 pms1Δ mutants showed lower spontaneous mutation rate compared with the single mutants in rapidly dividing cells. The combination the hsm3 mutation with all studied mutations characterized by different degree of increase of spontaneous mutagenesis in slowly dividing cells. The participation of the Hsm3p in spontaneous mutagenesis in slowly and activity dividing yeast cells is discussed. © 2004 Elsevier B.V. All rights reserved.},\r\nauthor_keywords={Adaptive mutation;  HSM3;  Spontaneous mutagenesis},\r\n}

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\n \n 2003\n \n \n (3)\n \n \n

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\n \n\n \n \n \n \n \n \n Genetics of P-Element Transposition into Drosophila melanogaster Centric Heterochromatin.\n \n \n \n \n\n\n \n Konev, A.; Yan, C.; Acevedo, D.; Kennedy, C.; Ward, E.; Lim, A.; Tickoo, S.; and Karpen, G.\n\n\n \n\n\n\n Genetics, 165(4): 2039-2053. 2003.\n cited By 24\n\n\n\n
\n\n\n\n \n \n $\"Genetics$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Konev20032039,\r\nauthor={Konev, A.Y. and Yan, C.M. and Acevedo, D. and Kennedy, C. and Ward, E. and Lim, A. and Tickoo, S. and Karpen, G.H.},\r\ntitle={Genetics of P-Element Transposition into Drosophila melanogaster Centric Heterochromatin},\r\njournal={Genetics},\r\nyear={2003},\r\nvolume={165},\r\nnumber={4},\r\npages={2039-2053},\r\nnote={cited By 24},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0346100693&partnerID=40&md5=93e62a1c39c894f5d6cbe8276ddc3e77},\r\naffiliation={Molec. and Cell Biology Laboratory, Salk Inst. for Biological Studies, San Diego, CA 92037, United States; Post Genomics, San Diego, CA 92121, United States; Department of Genetics, Case Western Reserve University, Cleveland, OH 44106, United States; Department of Genome Sciences, Lawrence Berkeley National Lab, 1 Cyclotron Rd., Berkeley, CA 94720, United States; University of Cambridge, Cambridge CB2 3EH, United Kingdom},\r\nabstract={Heterochromatin is a major component of higher eukaryotic genomes, but progress in understanding the molecular structure and composition of heterochromatin has lagged behind the production of relatively complete euchromatic genome sequences. The introduction of single-copy molecular-genetic entry points can greatly facilitate structure and sequence analysis of heterochromatic regions that are rich in repeated DNA. In this study, we report the isolation of 502 new P-element insertions into Drosophila melanogaster centric heterochromatin, generated in nine different genetic screens that relied on mosaic silencing (position-effect variegation, or PEV) of the yellow gene present in the transposon. The highest frequencies of recovery of variegating insertions were observed when centric insertions were used as the source for mobilization. We propose that the increased recovery of variegating insertions from heterochromatic starting sites may result from the physical proximity of different heterochromatic regions in germline nuclei or from the association of mobilizing elements with heterochromatin proteins. High frequencies of variegating insertions were also recovered when a potent suppressor of PEV (an extra Y chromosome) was present in both the mobilization and selection generations, presumably due to the effects of chromatin structure on P-element mobilization, insertion, and phenotypic selection. Finally, fewer variegating insertions were recovered after mobilization in females, in comparison to males, which may reflect differences in heterochromatin structure in the female and male germlines. FISH localization of a subset of the insertions confirmed that 98% of the variegating lines contain heterochromatic insertions and that these schemes produce a broader distribution of insertion sites. The results of these schemes have identified the most efficient methods for generating centric heterochromatin P insertions. In addition, the large collection of insertions produced by these screens provides molecular-genetic entry points for mapping, sequencing, and functional analysis of Drosophila heterochromatin.},\r\ncorrespondence_address1={Karpen, G.H.; Department of Genome Sciences, Lawrence Berkeley National Lab, 1 Cyclotron Rd., Berkeley, CA 94720, United States; email: karpen@fruitfly.org},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={14704184},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n Heterochromatin is a major component of higher eukaryotic genomes, but progress in understanding the molecular structure and composition of heterochromatin has lagged behind the production of relatively complete euchromatic genome sequences. The introduction of single-copy molecular-genetic entry points can greatly facilitate structure and sequence analysis of heterochromatic regions that are rich in repeated DNA. In this study, we report the isolation of 502 new P-element insertions into Drosophila melanogaster centric heterochromatin, generated in nine different genetic screens that relied on mosaic silencing (position-effect variegation, or PEV) of the yellow gene present in the transposon. The highest frequencies of recovery of variegating insertions were observed when centric insertions were used as the source for mobilization. We propose that the increased recovery of variegating insertions from heterochromatic starting sites may result from the physical proximity of different heterochromatic regions in germline nuclei or from the association of mobilizing elements with heterochromatin proteins. High frequencies of variegating insertions were also recovered when a potent suppressor of PEV (an extra Y chromosome) was present in both the mobilization and selection generations, presumably due to the effects of chromatin structure on P-element mobilization, insertion, and phenotypic selection. Finally, fewer variegating insertions were recovered after mobilization in females, in comparison to males, which may reflect differences in heterochromatin structure in the female and male germlines. FISH localization of a subset of the insertions confirmed that 98% of the variegating lines contain heterochromatic insertions and that these schemes produce a broader distribution of insertion sites. The results of these schemes have identified the most efficient methods for generating centric heterochromatin P insertions. In addition, the large collection of insertions produced by these screens provides molecular-genetic entry points for mapping, sequencing, and functional analysis of Drosophila heterochromatin.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Telomeric position effect in Drosophila melanogaster reflects a telomere length control mechanism.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Genetica, 117(2-3): 319-325. 2003.\n cited By 15\n\n\n\n
\n\n\n\n \n \n $\"Telomeric$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Cis- and trans-acting influences on telomeric position effect in Drosophila melanogaster detected with a subterminal transgene.\n \n \n \n \n\n\n \n Mason, J.; Konev, A.; Golubovsky, M.; and Biessmann, H.\n\n\n \n\n\n\n Genetics, 163(3): 917-930. 2003.\n cited By 20\n\n\n\n
\n\n\n\n \n \n $\"Cis-$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Mason2003917,\r\nauthor={Mason, J.M. and Konev, A.Y. and Golubovsky, M.D. and Biessmann, H.},\r\ntitle={Cis- and trans-acting influences on telomeric position effect in Drosophila melanogaster detected with a subterminal transgene},\r\njournal={Genetics},\r\nyear={2003},\r\nvolume={163},\r\nnumber={3},\r\npages={917-930},\r\nnote={cited By 20},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0037355012&partnerID=40&md5=367fe0b9630861c207f53b44a162b1fb},\r\naffiliation={Laboratory of Molecular Genetics, Natl. Inst. of Environ. Hlth. Sci., Res. Triangle Park, NC 27709-2233, United States; Developmental Biology Center, University of California, Irvine, CA 92697, United States; Division of Evolutionary Theory, Inst. of Sci. and Technology History, Russian Academy of Sciences, Saint Petersburg 199034, Russian Federation; Postgenomics Corporation, San Diego, CA 92121, United States},\r\nabstract={One model of telomeric position effect (TPE) in Drosophila melanogaster proposes that reporter genes in the vicinity of telomeres are repressed by subterminal telomere-associated sequences (TAS) and that variegation of these genes is the result of competition between the repressive effects of TAS and the stimulating effects of promoters in the terminal HeT-A transposon array. The data presented here support this model, but also suggest that TPE is more complex. Activity of a telomeric white reporter gene increases in response to deletion of some or all of the TAS on the homolog. Only transgenes next to fairly long HeT-A arrays respond to this trans-interaction. HeT-A arrays of 6-18 kb respond by increasing the number of dark spots on the eye, while longer arrays increase the background eye color or increase the number of spots sufficiently to cause them to merge. Thus, expression of a subtelomeric reporter gene is influenced by the telomere structure in cis and trans. We propose that the forces involved in telomere length regulation in Drosophila are the underlying forces that manifest themselves as TPE. In the wild-type telomere TAS may play an important role in controlling telomere elongation by repressing HeT-A promoter activity. Modulation of this repression by the homolog may thus regulate telomere elongation.},\r\ncorrespondence_address1={Biessmann, H.; Developmental Biology Center, University of California, Irvine, CA 92697, United States; email: hbiessma@uci.edu},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={12663532},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2002\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Efficient recovery of centric heterochromatin P-element insertions in Drosophila melanogaster.\n \n \n \n \n\n\n \n Yan, C.; Dobie, K.; Le, H.; Konev, A.; and Karpen, G.\n\n\n \n\n\n\n Genetics, 161(1): 217-229. 2002.\n cited By 26\n\n\n\n
\n\n\n\n \n \n $\"Efficient$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Yan2002217,\r\nauthor={Yan, C.M. and Dobie, K.W. and Le, H.D. and Konev, A.Y. and Karpen, G.H.},\r\ntitle={Efficient recovery of centric heterochromatin P-element insertions in Drosophila melanogaster},\r\njournal={Genetics},\r\nyear={2002},\r\nvolume={161},\r\nnumber={1},\r\npages={217-229},\r\nnote={cited By 26},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036259651&partnerID=40&md5=18e500458f5e7dad2498b96b5aa9f370},\r\naffiliation={Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, San Diego, CA 92037, United States; Department of Genetics, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106, United States; Isis Pharmaceuticals, 2292 Faraday Ave., Carlsbad, CA 92008, United States; Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd., San Diego, CA 92037, United States},\r\nabstract={Approximately one-third of the human and Drosophila melanogaster genomes are heterochromatic, yet we know very little about the structure and function of this enigmatic component of eukaryotic genomes. To facilitate molecular and cytological analysis of heterochromatin we introduced a yellow+ (y+)-marked P element into centric heterochromatin by screening for variegated phenotypes, that is, mosaic gene inactivation. We recovered &lt;110 P insertions with variegated yellow expression from ∼3500 total mobilization events. FISH analysis of 71 of these insertions showed that 69 (97%) were in the centric heterochromatin, rather than telomeres or euchromatin. High-resolution banding analysis showed a wide but nonuniform distribution of insertions within centric heterochromatin; variegated insertions were predominantly recovered near regions of satellite DNA. We successfully used inverse PCR to clone and sequence the flanking DNA for ∼63% of the insertions. BLAST analysis of the flanks demonstrated that either most of the variegated insertions could not be placed on the genomic scaffold, and thus may be inserted within novel DNA sequence, or that the flanking DNA hit multiple sites on the scaffold, due to insertions within different transposons. Taken together these data suggest that screening for yellow variegation is a very efficient method for recovering centric insertions and that a large-scale screen for variegated yellow P insertions will provide important tools for detailed analysis of centric heterochromatin structure and function.},\r\ncorrespondence_address1={Karpen, G.H.; Molecular Biology Laboratory, Salk Inst. for Biological Studies, 10010 N. Torrey Pines Rd., San Diego, CA 92037, United States; email: karpen@salk.edu},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={12019236},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n HSM2 (HMO1) gene participates in mutagenesis control in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Alekseev, S.; Kovaltsova, S.; Fedorova, I.; Gracheva, L.; Evstukhina, T.; Peshekhonov, V.; and Korolev, V.\n\n\n \n\n\n\n DNA Repair, 1(4): 287-297. 2002.\n cited By 16\n\n\n\n
\n\n\n\n \n \n $\"HSM2$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Alekseev2002287,\r\nauthor={Alekseev, S.Yu. and Kovaltsova, S.V. and Fedorova, I.V. and Gracheva, L.M. and Evstukhina, T.A. and Peshekhonov, V.T. and Korolev, V.G.},\r\ntitle={HSM2 (HMO1) gene participates in mutagenesis control in yeast Saccharomyces cerevisiae},\r\njournal={DNA Repair},\r\nyear={2002},\r\nvolume={1},\r\nnumber={4},\r\npages={287-297},\r\ndoi={10.1016/S1568-7864(02)00005-8},\r\nnote={cited By 16},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0037193545&doi=10.1016%2fS1568-7864%2802%2900005-8&partnerID=40&md5=0bf91436b9301394dd9eca155541961a},\r\naffiliation={Laboratory of Eucaryote Genetics, Div. of Molec. and Radiat. Biophys., Petersburg Nuclear Physics Institute, 188350 Orlova Roscha, Gatchina, Russian Federation},\r\nabstract={We have previously reported about a new Saccharomyces cerevisiae mutation, hsm2-1, that results in increase of both spontaneous and UV-induced mutation frequencies but does not alter UV-sensitivity. Now HSM2 gene has been genetically and physically mapped and identified as a gene previously characterized as HMO1, a yeast homologue of human high mobility group genes HMG1/2. We found that hsm2 mutant is slightly deficient in plasmid-borne mismatch repair. We tested UV-induced mutagenesis in double mutants carrying hsm2-1 mutation and a mutation in a gene of principal damaged DNA repair pathways (rad2 and rev3) or in a mismatch repair gene (pms1 and recently characterized in our laboratory hsm3). The frequency of UV-induced mutations in hsm2 rev3 was not altered in comparison with single rev3 mutant. In contrast, the interaction of hsm2-1 with rad2 and pms1 was characterized by an increased frequency of UV-induced mutations in comparison with single rad2 and pms1 mutants. The UV-induced mutation frequency in double hsm2 hsm3 mutant was lower than in the single hsm2 and hsm3 mutants. The role of the HSM2 gene product in control of mutagenesis is discussed. © 2002 Elsevier Science B.V. All rights reserved.},\r\nauthor_keywords={DNA repair;  hsm2 and hmo1 mutants;  Mutagenesis;  Yeast},\r\n}

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\n \n 2001\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Terminal retrotransposons activate a subtelomeric white transgene at the 2L telomere in Drosophila.\n \n \n \n \n\n\n \n Golubovsky, M.; Konev, A.; Walter, M.; Biessmann, H.; and Mason, J.\n\n\n \n\n\n\n Genetics, 158(3): 1111-1123. 2001.\n cited By 52\n\n\n\n
\n\n\n\n \n \n $\"Terminal$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Golubovsky20011111,\r\nauthor={Golubovsky, M.D. and Konev, A.Y. and Walter, M.F. and Biessmann, H. and Mason, J.M.},\r\ntitle={Terminal retrotransposons activate a subtelomeric white transgene at the 2L telomere in Drosophila},\r\njournal={Genetics},\r\nyear={2001},\r\nvolume={158},\r\nnumber={3},\r\npages={1111-1123},\r\nnote={cited By 52},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0034918688&partnerID=40&md5=d6f298ee1b025ddbb53613288777432d},\r\naffiliation={Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, RTP, NC 27709-2233, United States; Developmental Biology Center, University of California, Irvine, CA 92697, United States; Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, 111 Alexander Dr, RTP, NC 27709-2233, United States; Division of Evolutionary Theory, Institute of Science and Technology History, Russian Academy of Sciences, St. Petersburg 199034, Russian Federation; Molecular Biology and Virology Laboratory, Salk Institute, San Diego, CA 92037, United States},\r\nabstract={Genetically marked P elements inserted into the subtelomeric satellites of Drosophila show repression and variegation of the reporter gene. One such white+ reporter, inserted between the subtelomeric satellite and the terminal HeT-A array in the left arm of chromosome 2 (2L), is sensitive to its context; changes in the structure of the telomere region can be identified by changes in eye color. Addition of HeT-A or TART elements to the 2L terminus increases w+ expression, and loss of sequence from the end decreases expression. This indicates that the telomeric retrotransposons in Drosophila have an activating influence on the repressed subterminal reporter gene. Changes in eye color due to altered expression of the transgene also allow the detection of interactions between homologous telomeres. The 2L arms that terminate in long HeT-A/TART arrays showed increased expression of the subterminal w+ transgene when the terminal repeats on the homologue are absent or markedly shorter. We propose that the chromatin structure of the terminal HeT-A/TART array and the activity of a putative promoter/enhancer element on HeT-A are affected by telomeric interactions. Such trans-activation may reflect control over HeT-A transcription and, thus, transposition activity.},\r\ncorrespondence_address1={Mason, J.M.; Laboratory of Molecular Genetics, Natl. Inst. of Envtl. Hlth. Sciences, 111 Alexander Dr., Res. Triangle Park, NC 27709-2233, United States; email: masonj@niehs.nih.gov},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={11454760},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The REC41 gene of Saccharomyces cerevisiae: Isolation and genetic analysis.\n \n \n \n \n\n\n \n Chepurnaya, O.; Kozhina, T.; Peshekhonov, V.; and Korolev, V.\n\n\n \n\n\n\n Mutation Research - DNA Repair, 486(1): 41-52. 2001.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Chepurnaya200141,\r\nauthor={Chepurnaya, O.V. and Kozhina, T.N. and Peshekhonov, V.T. and Korolev, V.G.},\r\ntitle={The REC41 gene of Saccharomyces cerevisiae: Isolation and genetic analysis},\r\njournal={Mutation Research - DNA Repair},\r\nyear={2001},\r\nvolume={486},\r\nnumber={1},\r\npages={41-52},\r\ndoi={10.1016/S0921-8777(01)00079-9},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035811265&doi=10.1016%2fS0921-8777%2801%2900079-9&partnerID=40&md5=da6d4186dbc1781b384e14bc9d1619e3},\r\naffiliation={Laboratory of Eukaryotic Genetics, Division of Molecular and Radiation Biophysics, Petersburg Nuclear Physics Institute, RAS, Gatchina, 188350 Leningrad, Russian Federation},\r\nabstract={Recombination-deficient strains have been proven useful for the understanding of the genetic control of homologous recombination. As the genetic screens used to isolate recombination-deficient (rec-) yeast mutants have not been saturated, we sought to develop a simple colony color assay to identify mutants with low or elevated rates of recombination. Using this system we isolated a collection of rec- mutants. We report the characterization of the REC41 gene identified in this way. REC41 is required for normal levels of interplasmid recombination and γ-ray induced mitotic interchromosomal recombination. The rec41-1 mutant failed to grow at 37°C. Microscopic analysis of plated cells showed that 45-50% of them did not form visible colonies at permissive temperature. Haploid cells of the rec41 mutant show the same γ-ray sensitivity as wild type ones. However, the diploid rec41 mutant shows γ-ray sensitivity which is comparable with heterozygous REC41/rec41-1 diploid cells. This fact indicates semidominance of the rec41-1 mutation. Diploid strains homozygous for the rec41 rad52 mutations had the same γ-ray sensitivity as single rad52 diploids and exhibited dramatically decreased growth rate. The expression of the HO gene does not lead to inviability of rec41 cells. The rec41 mutation has an effect on meiosis, likely meiotic recombination, even in the heterozygous state. We cloned the REC41 gene. Sequence analysis revealed that the REC41 gene is encoded by ORF YDR245w. Earlier, this ORF was attributed to MNN10, BED1, SLC2, CAX5 genes. Two multicopy plasmids with suppressers of the rec41-1 mutation (pm21 and pm32) were isolated. The deletion analysis showed that only DNA fragments with the CDC43 and HAC1 genes can partially complement the rec41-1 mutation. © 2001 Published by Elsevier Science B.V.},\r\nauthor_keywords={DNA repair;  Homologous recombination;  Rec- Mutants;  Yeast},\r\n}

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\n \n 2000\n \n \n (6)\n \n \n

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\n \n\n \n \n \n \n \n \n RAD29 and RAD31, new genes of the yeast saccharomyces cerevisiae involved in dna repair control: ii. determining possible functions of these genes.\n \n \n \n \n\n\n \n Kozhin, S.; Kozhina, T.; Latypov, V.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 36(8): 1025-1032. 2000.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"RAD29$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhin20001025,\r\nauthor={Kozhin, S.A. and Kozhina, T.N. and Latypov, V.F. and Korolev, V.G.},\r\ntitle={RAD29 and RAD31, new genes of the yeast saccharomyces cerevisiae involved in dna repair control: ii. determining possible functions of these genes},\r\njournal={Genetika},\r\nyear={2000},\r\nvolume={36},\r\nnumber={8},\r\npages={1025-1032},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0034242186&partnerID=40&md5=3884fe6316a30161823e667596be7408},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, St. Petersburg, 188350, Russian Federation},\r\nabstract={Possible functions of previously described genes RAD29 and RAD31 involved in DNA repair were determined by analyzing the interaction between these genes and mutations in the genes of the three basic epistatic groups: RAD3 (nucleotide excision repair), RAD6 (error-prone mutagenic repair system), RAD52 (recombination repair pathway), and also the apnl mutation that blocks the synthesis of major AP endonuclease (base excision repair). The results obtained in these studies and the estimation of the capability for excision repair of lesions induced by 8-metoxipsoralen and subsequent exposure to long-wavelength UV light in mutants for these genes led to the assumption that the RAD29 and RAD31 genes are involved in yeast DNA repair control.},\r\ncorrespondence_address1={Kozhin, S.A.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, St. Petersburg, 188350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={11033772},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

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\n\n\n

\n \n\n \n \n \n \n \n \n RAD29 and RAD31, new genes of yeast saccharomyces cerevisiae involved in DNA repair control: isolation and genetic characterization of mutants.\n \n \n \n \n\n\n \n Kozhina, T.; Kozhin, S.; Latypov, V.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 36(6): 767-773. 2000.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"RAD29$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Kozhina2000767,\r\nauthor={Kozhina, T.N. and Kozhin, S.A. and Latypov, V.F. and Korolev, V.G.},\r\ntitle={RAD29 and RAD31, new genes of yeast saccharomyces cerevisiae involved in DNA repair control: isolation and genetic characterization of mutants},\r\njournal={Genetika},\r\nyear={2000},\r\nvolume={36},\r\nnumber={6},\r\npages={767-773},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0034201604&partnerID=40&md5=de2d6980b72b416fb010ef22c4672b42},\r\naffiliation={Konstantinov Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad ablast, 188350, Russian Federation},\r\nabstract={Base excision repair (BER) and nucleotide excision repair (NER) are two main cellular responses to DNA damage induced by various physical and chemical factors. After exposure of the strain that carries the NER-blocking radl mutation to UV light, several mutants hypersensitive to the UV light lethal action and simultaneously sensitive to methylmethanesulphonate (MMS) were isolated. Two of these mutants (Uvs64 and Uvs212) were examined in detail. The mutants were found to carry recessive, monogenically inherited lesions that had pleiotropic, though different, phenotypes: both mutants were also sensitive to nitrous acid (HNO2), whereas Uvs212 was sensitive to hydrogen peroxide as well. Moreover, the homozygote for the uvs212 mutation, but not for uvs64, blocks the sporulation. Since the mutations examined were not allelic to any of the known rod mutations that cause MMS sensitivity or to each other, it is concluded that two new genes involved in the control of yeast DNA repair were detected. Furthermore, these genes were mapped to different regions of the right arm of chromosome 2 where repair genes were not found. Thus, two new genes, designated RAD29(UVS64) and RAD31(UVS212) and probably involved in base excision repair, were identified.},\r\ncorrespondence_address1={Kozhina, T.N.; Konstantinov Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad ablast, 188350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={10923258},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n RAD29 and RAD31, new genes of the yeast Saccharomyces cerevisiae involved in DNA repair control: Determining possible functions of these genes.\n \n \n \n \n\n\n \n Kozhin, S.; Kozhina, T.; Latypov, V.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 36(8): 845-852. 2000.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"RAD29$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Kozhin2000845,\r\nauthor={Kozhin, S.A. and Kozhina, T.N. and Latypov, V.F. and Korolev, V.G.},\r\ntitle={RAD29 and RAD31, new genes of the yeast Saccharomyces cerevisiae involved in DNA repair control: Determining possible functions of these genes},\r\njournal={Russian Journal of Genetics},\r\nyear={2000},\r\nvolume={36},\r\nnumber={8},\r\npages={845-852},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-22244457728&partnerID=40&md5=7606f6e3efeb00e0926ff463af91374e},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, St. Petersburg, 188350, Russian Federation},\r\nabstract={Possible functions of previously described genes RAD29 and RAD31 involved in DNA repair were determined by analyzing the interaction between these genes and mutations in the genes of the three basic epistatic groups: RAD3 (nucleotide excision repair), RAD6 (error-prone mutagenic repair system), RAD52 (recombination repair pathway), and also the apn1 mutation that blocks the synthesis of major AP endonuclease (base excision repair). The results obtained in these studies and the estimation of the capability for excision repair of lesions induced by 8-metoxipsoralen and subsequent exposure to long-wavelength UV light in mutants for these genes led to the assumption that the RAD29 and RAD31 genes are involved in yeast DNA repair control. © 2000 MAIK "Nauka/Interperiodica".},\r\ncorrespondence_address1={Kozhin, S.A.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, St. Petersburg, 188350, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Control of telomere elongation and telomeric silencing in Drosophila melanogaster.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Genetica, 109(1-2): 61-70. 2000.\n cited By 26\n\n\n\n
\n\n\n\n \n \n $\"Control$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n RAD29 and RAD31, new genes of yeast Saccharomyces cerevisiae involved in DNA repair control: Isolation and genetic characterization of mutants.\n \n \n \n \n\n\n \n Kozhina, T.; Kozhin, S.; Latypov, V.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 36(6): 627-633. 2000.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"RAD29$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina2000627,\r\nauthor={Kozhina, T.N. and Kozhin, S.A. and Latypov, V.F. and Korolev, V.G.},\r\ntitle={RAD29 and RAD31, new genes of yeast Saccharomyces cerevisiae involved in DNA repair control: Isolation and genetic characterization of mutants},\r\njournal={Russian Journal of Genetics},\r\nyear={2000},\r\nvolume={36},\r\nnumber={6},\r\npages={627-633},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-22244489109&partnerID=40&md5=82291901c501e87cb24726aaa2df271e},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad oblast, 188350, Russian Federation},\r\nabstract={Base excision repair (BER) and nucleotide excision repair (NER) are two main cellular responses to DNA damage induced by various physical and chemical factors. After exposure of the strain that carries the NER-blocking rad2 mutation to UV light, several mutants hypersensitive to UV light lethal action and simultaneously sensitive to methylmethanesulphonate (MMS) were isolated. Two of these mutants (Uvs64 and Uvs212) were examined in detail. The mutants were found to carry recessive, monogenically inherited lesions that had pleiotropic, though different, phenotypes: both mutants were also sensitive to nitrous acid (HNO2), whereas Uvs212 was sensitive to hydrogen peroxide as well. Moreover, the homozygote for the uvs212 mutation, but not for uvs64, blocks sporulation. Since the mutations examined were not allelic to any of the known rad mutations that cause MMS sensitivity or to each other, it is concluded that two new genes involved in the control of yeast DNA repair were detected. Furthermore, these genes were mapped to different regions of the right arm of chromosome 2 where repair genes were not found. Thus, two new genes, designated RAD29 (UVS64) and RAD31 (UVS212) and probably involved in base excision repair, were identified. © 2000 MAIK "Nauka/Interperiodica".},\r\ncorrespondence_address1={Kozhina, T.N.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad oblast, 188350, Russian Federation},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The yeast HSM3 gene is involved in DNA mismatch repair in slowly dividing cells [2].\n \n \n \n \n\n\n \n Fedorova, I.; Kovaltzova, S.; and Korolev, V.\n\n\n \n\n\n\n Genetics, 154(1): 495-496. 2000.\n cited By 7\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Fedorova2000495,\r\nauthor={Fedorova, I.V. and Kovaltzova, S.V. and Korolev, V.G.},\r\ntitle={The yeast HSM3 gene is involved in DNA mismatch repair in slowly dividing cells [2]},\r\njournal={Genetics},\r\nyear={2000},\r\nvolume={154},\r\nnumber={1},\r\npages={495-496},\r\nnote={cited By 7},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0033978882&partnerID=40&md5=4c76edf56be07b81ebb737931c7e5161},\r\naffiliation={B. P. Konstantinov Petersburg N., Russian Academy of Science, 188350 Gatchina, Leningrad District, Russian Federation; Petersburg Nuclear Physics Institute, Div. of Molec. and Radiat. Biophys., RAS, 188350, Gatchina, Leningrad District, Russian Federation},\r\ncorrespondence_address1={Korolev, V.G.; Petersburg Nuclear Physics Institute, Div. of Molec./Radiation Biophysics, RAS, 188350 Gatchina, Russian Federation; email: Ige@omrb.pnpi.spb.ru},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={10681183},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Letter},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1999\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n A new recombinational DNA repair gene from Schizosaccharomyces pombe with homology to Escherichia coli RecA.\n \n \n \n \n\n\n \n Khasanov, F.; Savchenko, G.; Bashkirova, E.; Korolev, V.; Heyer, W.; and Bashkirov, V.\n\n\n \n\n\n\n Genetics, 152(4): 1557-1572. 1999.\n cited By 56\n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Khasanov19991557,\r\nauthor={Khasanov, F.K. and Savchenko, G.V. and Bashkirova, E.V. and Korolev, V.G. and Heyer, W.-D. and Bashkirov, V.I.},\r\ntitle={A new recombinational DNA repair gene from Schizosaccharomyces pombe with homology to Escherichia coli RecA},\r\njournal={Genetics},\r\nyear={1999},\r\nvolume={152},\r\nnumber={4},\r\npages={1557-1572},\r\nnote={cited By 56},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0344246905&partnerID=40&md5=9e5d7978807a0135a92e83b23f1091c0},\r\naffiliation={Institute of Gene Biology, Russian Academy of Sciences, Moscow 117 984, Russian Federation; Section of Microbiology, University of California, Davis, CA 95616, United States; St. Petersburg Nucl. Phys. Institute, Gatchina 188 350, Russian Federation; Institute for General Microbiology, University of Bern, CH-3012 Bern, Switzerland; Section of Microbiology, University of California, Davis, 1 Shields Ave., Davis, CA 95616, United States},\r\nabstract={A new DNA repair gene from Schizosaccharomyces pombe with homology to RecA was identified and characterized. Comparative analysis showed highest similarity to Saccharomyces cerevisiae Rad55p. rhp55+ (rad homologue pombe 55) encodes a predicted 350-amino-acid protein with an Mr of 38,000. The rhp55Δ mutant was highly sensitive to methyl methanesulfonate (MMS), ionizing radiation (IR), and, to a lesser degree, UV. These phenotypes were enhanced at low temperatures, similar to deletions in the S. cerevisiae RAD55 and RAD57 genes. Many rhp55A cells were elongated with aberrant nuclei and an increased DNA content. The rhp55 mutant showed minor deficiencies in meiotic intra- and intergenic recombination. Sporulation efficiency and spore viability were significantly reduced. Double-mutant analysis showed that rhp55+ acts in one DNA repair pathway with rhp51+ and rhp54+, homologs of the budding yeast RAD51 and RAD54 genes, respectively. However, rhp55+ is in a different epistasis group for repair of UV-, MMS-, or γ-ray-induced DNA damage than is rad22+, a putative RAD52 homolog of fission yeast. The structural and functional similarity suggests that rhp55+ is a homolog of the S. cerevisiae RAD55 gene and we propose that the functional diversification of RecA-like genes in budding yeast is evolutionarily conserved.},\r\ncorrespondence_address1={Heyer, W.-D.; Section of Microbiology, University of California, 1 Shields Ave., Davis, CA 95616, United States; email: wdheyer@ucdavis.edu},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={10430583},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1998\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n The yeast HSM3 gene acts in one of the mismatch repair pathways.\n \n \n \n \n\n\n \n Fedorova, I.; Gracheva, L.; Kovaltzova, S.; Evstuhina, T.; Alekseev, S.; and Korolev, V.\n\n\n \n\n\n\n Genetics, 148(3): 963-973. 1998.\n cited By 24\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Fedorova1998963,\r\nauthor={Fedorova, I.V. and Gracheva, L.M. and Kovaltzova, S.V. and Evstuhina, T.A. and Alekseev, S.Yu. and Korolev, V.G.},\r\ntitle={The yeast HSM3 gene acts in one of the mismatch repair pathways},\r\njournal={Genetics},\r\nyear={1998},\r\nvolume={148},\r\nnumber={3},\r\npages={963-973},\r\nnote={cited By 24},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0031961248&partnerID=40&md5=bc4ee76f1bcf6cb3c0bdbb2d523f6f8d},\r\naffiliation={B. P. Konstantinov Petersburg N., Russian Academy of Science, 188350 Gatchina, Russian Federation; Petersburg Nuclear Physics Institute, Div. of Molec. and Radiat. Biophys., Russian Academy of Science, 188350, Gatchina, Russian Federation},\r\nabstract={Mutants with enhanced spontaneous mutability (hsm) to canavanine resistance were induced by N-methyl-N-nitrosourea in Saccharomyces cerevisiae. One bearing the hsm3-1 mutation was used for this study. This mutation does not increase sensitivity to the lethal action of different mutagens. The hsm3-1 mutation produces a mutator phenotype, enhancing the rates of spontaneous mutation to canavanine resistance and reversions of lys1-1 and his1-7. This mutation increases the rate of intragenic mitotic recombination at the ADE2 gene. The ability of the hsm3 mutant to correct DNA heteroduplex is reduced in comparison with the wild-type strain. All these phenotypes are similar to ones caused by pms1, mlh1, and msh2 mutations. In contrast to these mutations, hsm3-1 increases the frequency of ade mutations induced by 6-HAP and UV light. Epistasis analysis of double mutants shows that the PMS1 and HSM3 genes control different mismatch repair systems. The HSM3 gene maps to the right arm of chromosome II, 25 cM distal to the HIS7 gene. Strains that bear a deleted open reading frame YBR272c have the genetic properties of the hsm3 mutant. The HSM3 product shows weak similarity to predicted products of the yeast MSH genes (homologs of the Escherichia coli mutS gene). The HSM3 gene may be a member of the yeast MutS homolog family, but its function in DNA metabolism differs from the functions of other yeast MutS homologs.},\r\ncorrespondence_address1={Korolev, V.G.; Petersburg Nuclear Physics Institute, Div. of Molec. and Radiat. Biophys., Russian Academy of Science, 188350 Gatchina, Leningrad District, Russian Federation; email: lge@omrb.pnpi.spb.ru},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={9539417},\r\nlanguage={English},\r\nabbrev_source_title={Genetics},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1997\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n The RAD29 gene: Map position on the right arm of chromosome II.\n \n \n \n \n\n\n \n Kozhin, S.; Kozhina, T.; and Korolev, V.\n\n\n \n\n\n\n Yeast, 13(5): 489-490. 1997.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Kozhin1997489,\r\nauthor={Kozhin, S.A. and Kozhina, T.N. and Korolev, V.G.},\r\ntitle={The RAD29 gene: Map position on the right arm of chromosome II},\r\njournal={Yeast},\r\nyear={1997},\r\nvolume={13},\r\nnumber={5},\r\npages={489-490},\r\ndoi={10.1002/(SICI)1097-0061(199704)13:5<489::AID-YEA108>3.0.CO;2-3},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0030984637&doi=10.1002%2f%28SICI%291097-0061%28199704%2913%3a5%3c489%3a%3aAID-YEA108%3e3.0.CO%3b2-3&partnerID=40&md5=53a4527addb6ead01b658d92115bec35},\r\naffiliation={Dept. of Molec. and Radiat. Biophys., Petersburg Nuclear Physics Institute, Russian Academy of Science, Gatchina, Leningrad distr., 188350, Russian Federation},\r\nauthor_keywords={Genetic analysis;  Mapping;  RAD29;  Repair and recombination genes;  Saccharomyces cerevisiae},\r\ncorrespondence_address1={Kozhin, S.A.; Dept. Molecular/Radiation Biophysics, Petersburg Nuclear Physics Institute, Gatchina, Leningrad distr, 188350, Russian Federation},\r\nissn={0749503X},\r\ncoden={YESTE},\r\npubmed_id={9153760},\r\nlanguage={English},\r\nabbrev_source_title={YEAST},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1996\n \n \n (3)\n \n \n

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\n \n\n \n \n \n \n \n \n The saccharomyces cerevisiae yeast strain for testing environmental mutagens based on the interaction between rad2 and himl mutations.\n \n \n \n \n\n\n \n Kovaptsova, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 32(3): 366-372. 1996.\n cited By 7\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kovaptsova1996366,\r\nauthor={Kovaptsova, S.B. and Korolev, V.G.},\r\ntitle={The saccharomyces cerevisiae yeast strain for testing environmental mutagens based on the interaction between rad2 and himl mutations},\r\njournal={Genetika},\r\nyear={1996},\r\nvolume={32},\r\nnumber={3},\r\npages={366-372},\r\nnote={cited By 7},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0030101572&partnerID=40&md5=37a68d4064520877dacabbe978d1cec2},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nabstract={The interaction between mutations at the RAD2 and HIM1 genes was studied. The RAD2 gene encodes endonuclease involved in nucleotide excision repair. Mutants at this gene are highly sensitive to the lethal effect of a variety of mutagens. The product of the ///A/7 gene is needed for correction of mismatched bases and repair of premutational DN A damage. Mutations in this gene lead to the formation of the mutator phenotype and high sensitivity to induced mutagenesis. The double rad2 himl mutant manifested the synergic type of interaction. The level of UV-induced mutagenesis in the double mutant was five times higher than in single mutants, and the absolute yield of forward mutations in five genes controlling adenine biosynthesis was 1 to 2%. UV-induced mutagenesis was increased, at low doses, by several orders of magnitude in the double mutant, compared to the wild-type strain. The high level of mutagenesis in this mutant was caused by ethyl and methyl methanesulfonate. These properties of the stock with the double rad.2 himl mutation makes it promising as a tester in analysis of the gene toxicity of different substances.},\r\ncorrespondence_address1={Kovaptsova, S.B.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={8723629},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutator genes of the yeast saccharomyces cerevisiae interaction between mutations him and hsm and mutations blocking three principal pathways of induced dna damage repair.\n \n \n \n \n\n\n \n Gracheva, L.; Evstyukhina, T.; Kovaptsova, S.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 32(7): 922-926. 1996.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Mutator$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva1996922,\r\nauthor={Gracheva, L.M. and Evstyukhina, T.A. and Kovaptsova, S.V. and Fedorova, I.V. and Korolev, V.G.},\r\ntitle={Mutator genes of the yeast saccharomyces cerevisiae interaction between mutations him and hsm and mutations blocking three principal pathways of induced dna damage repair},\r\njournal={Genetika},\r\nyear={1996},\r\nvolume={32},\r\nnumber={7},\r\npages={922-926},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0030179760&partnerID=40&md5=6cf5e7cc4b26311f851ea7465195ec14},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, St. Petersburg, Leningradskaya oblast, J88350, Russian Federation},\r\nabstract={During recent years, genes controlling mutation in higher eukaryotes have been found to be involved actively in carcinoma regeneration in cells. In this respect, studying the genetic control of mutagenesis becomes a key direction of research into mechanisms responsible for cancer generation. The results of studying interaction of mutations in the HSM3 and HSM6 genes, controlling spontaneous and induced mutagenesis in yeasts, and mutations impairing three known pathways of DNA damage repair in this microorganism, are described in this work. It was shown that mutation rev3 completely blocks UV-induced mutagenesis in all mutants studied. On the other hand, mutation rad2 synergistically interacts with mutations him!, hsml, hsm3, hsmo, and hsm2, thus enhancing the frequency of UV-induced mutagenesis in double mutants multiple times. Mutations him2 and him3 manifested epistatic interaction with mutation rad2. With mutation rad54, the interaction was epistatic for mutations himl and hsm2 and was additive for mutations hsml, him.2, and him3. On the basis of the data obtained, we developed a scheme for the appearance of mismatch bases in the process of repair of UV-induced DNA damage.},\r\ncorrespondence_address1={Gracheva, L.M.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, St. Petersburg, Leningradskaya oblast, J88350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutator Genes of the Yeast Saccharomyces cerevisiae: I. Repair of Artificial Heteroduplexes in Mutants him and hsm.\n \n \n \n \n\n\n \n Gracheva, L.; Evstyukhina, T.; Koval'tsova, S.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 32(7): 801-804. 1996.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Mutator$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva1996801,\r\nauthor={Gracheva, L.M. and Evstyukhina, T.A. and Koval'tsova, S.V. and Fedorova, I.V. and Korolev, V.G.},\r\ntitle={Mutator Genes of the Yeast Saccharomyces cerevisiae: I. Repair of Artificial Heteroduplexes in Mutants him and hsm},\r\njournal={Russian Journal of Genetics},\r\nyear={1996},\r\nvolume={32},\r\nnumber={7},\r\npages={801-804},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-1542398329&partnerID=40&md5=862f899fd42e15de7a44cb9b8028e9ae},\r\naffiliation={St. Petersburg Inst. of Nucl. Phys., Russian Academy of Sciences, Leningradskaya oblast, 188350, Russian Federation},\r\nabstract={Repair of artificial heteroduplexes in plasmid DNA by mutants of the yeast Saccharomyces cerevisiae possessing the mutator phenotype was studied. Mutants for genes HSM3 and HSM6 were shown to repair mismatched bases with a lower efficiency than the wild-type strain. The extent of the decrease in heteroduplex repair efficiency in these mutants is comparable to that in mutant pms1, which is known to block the principal repair pathway for mismatched bases in yeasts. Mutations hsm1-1 and hsm2-1 also affect one branch of DNA mismatched base repair characterized by a high allele specificity. Another two mutator genes, HIM2 and HIM3, probably control repair of mismatched bases directed by DNA strand breaks.},\r\ncorrespondence_address1={Gracheva, L.M.; St. Petersburg Inst. of Nucl. Phys., Russian Academy of Sciences, Leningradskaya oblast, 188350, Russian Federation},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1995\n \n \n (5)\n \n \n

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\n \n\n \n \n \n \n \n \n RAD58 (XRS4)-A new gene in the RAD52 epistasis group.\n \n \n \n \n\n\n \n Chepurnaya, O.; Kozhin, S.; Peshekhonov, V.; and Korolev, V.\n\n\n \n\n\n\n Current Genetics, 28(3): 274-279. 1995.\n cited By 15\n\n\n\n
\n\n\n\n \n \n $\"RAD58$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Chepurnaya1995274,\r\nauthor={Chepurnaya, O.V. and Kozhin, S.A. and Peshekhonov, V.T. and Korolev, V.G.},\r\ntitle={RAD58 (XRS4)-A new gene in the RAD52 epistasis group},\r\njournal={Current Genetics},\r\nyear={1995},\r\nvolume={28},\r\nnumber={3},\r\npages={274-279},\r\ndoi={10.1007/BF00309787},\r\nnote={cited By 15},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0029143250&doi=10.1007%2fBF00309787&partnerID=40&md5=5d662c2b0f14c7feef57fa4082a0b8c9},\r\naffiliation={Laboratory of Genetics of Eukaryotes, Department of Molecular and Radiation Biophysics, Petersburg Nuclear Physics Institute, Academy of Sciences of Russia, Gatchina, 188350, Russian Federation},\r\nabstract={The RAD58 (XRS4) gene of Saccharomyces cerevisiae has been previously identified as a DNA repair gene. In this communication, we show that RAD58 also encodes an essential meiotic function. The spore inviability of rad58 strains is not rescued by a spo13 mutation. The rad50 mutation suppresses spore inviability of a spo13 rad58 strain suggesting that RAD58 acts after RAD50 in meiotic recombination. The rad58-4 mutation does not prevent mitotic recombination events. Haploid rad58 cells fail to carry out G2-repair of gamma-induced lesions, whereas rad58/rad58 diploids are able to perform some diploid-specific repair of these lesions. © 1995 Springer-Verlag.},\r\nauthor_keywords={RAD58;  Recombination;  Repair;  Yeast},\r\ncorrespondence_address1={Korolev, V.G.; Laboratory of Genetics of Eukaryotes, Department of Molecular and Radiation Biophysics, Petersburg Nuclear Physics Institute, Academy of Sciences of Russia, Gatchina, 188350, Russian Federation},\r\npublisher={Springer-Verlag},\r\nissn={01728083},\r\ncoden={CUGED},\r\npubmed_id={8529274},\r\nlanguage={English},\r\nabbrev_source_title={Curr Genet},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Gene RAD58(XRS4): Mapping to the right arm of chromosome XIII.\n \n \n \n \n\n\n \n Kozhin, S.; Chepurnaya, O.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 31(2): 281-282. 1995.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Gene$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhin1995281,\r\nauthor={Kozhin, S.A. and Chepurnaya, O.V. and Korolev, V.G.},\r\ntitle={Gene RAD58(XRS4): Mapping to the right arm of chromosome XIII},\r\njournal={Genetika},\r\nyear={1995},\r\nvolume={31},\r\nnumber={2},\r\npages={281-282},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0029246467&partnerID=40&md5=e1d2ee3d905aa1ab1aa85d643bb3781b},\r\naffiliation={Konstantinov Inst.of Nuclear Physics, Russian Academy of Sciences, Gatchina 188350, Russian Federation},\r\nabstract={This report presents the results of mapping of Saccharomyces cerevisiae gene RAD58(XRS4) to the right arm of chromosome XIII at a distance of 48 cM proximal to the gene ADE4.},\r\ncorrespondence_address1={Kozhin, S.A.; Konstantinov Inst.of Nuclear Physics, Russian Academy of Sciences, Gatchina 188350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={7721072},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n XIII. Yeast mapping reports. The RAD58 (XRS4) gene: Map position on the right arm of chromosome XIII.\n \n \n \n \n\n\n \n Kozhin, S.; Chepurnaya, O.; and Korolev, V.\n\n\n \n\n\n\n Yeast, 11(12): 1211-1213. 1995.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"XIII.$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhin19951211,\r\nauthor={Kozhin, S.A. and Chepurnaya, O.V. and Korolev, V.G.},\r\ntitle={XIII. Yeast mapping reports. The RAD58 (XRS4) gene: Map position on the right arm of chromosome XIII},\r\njournal={Yeast},\r\nyear={1995},\r\nvolume={11},\r\nnumber={12},\r\npages={1211-1213},\r\ndoi={10.1002/yea.320111211},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0029134539&doi=10.1002%2fyea.320111211&partnerID=40&md5=852bf43488d704547a3a2556b7171e2f},\r\naffiliation={Department of Molecular and Radiation Biophysics, Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nauthor_keywords={genetic analysis;  mapping;  repair and recombination genes;  Saccharomyces cerevisiae},\r\ncorrespondence_address1={Kozhin, S.A.; Department of Molecular and Radiation Biophysics, Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nissn={0749503X},\r\npubmed_id={8619319},\r\nlanguage={English},\r\nabbrev_source_title={Yeast},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Analysis of maintenance of redundant genetic structures in the yeast Saccharomyces cerevisiae: Effects of mutations cdc28-srm and srm1.\n \n \n \n \n\n\n \n Smirnova, M.; Arman, I.; Devin, A.; Peshekhonov, V.; Chepurnaya, O.; Koltovaya, N.; and Troitskaya, E.\n\n\n \n\n\n\n Genetika, 31(4): 464-470. 1995.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Analysis$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Smirnova1995464,\r\nauthor={Smirnova, M.E. and Arman, I.P. and Devin, A.B. and Peshekhonov, V.T. and Chepurnaya, O.V. and Koltovaya, N.A. and Troitskaya, E.N.},\r\ntitle={Analysis of maintenance of redundant genetic structures in the yeast Saccharomyces cerevisiae: Effects of mutations cdc28-srm and srm1},\r\njournal={Genetika},\r\nyear={1995},\r\nvolume={31},\r\nnumber={4},\r\npages={464-470},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0028990067&partnerID=40&md5=62b96e0a8216bf45c337ee2e43c5f3d4},\r\naffiliation={Institute of Molecular Genetics, Russian Academy of Sciences, Moscow 123182, Russian Federation},\r\nabstract={The effects of nuclear gene mutations cdc28-srm and srm1 on the maintenance of various recombinant facultative genetic structures (FGSs) in Saccharomyces cerevisiae were studied. These structures are ARS1 TRP1 minicoils, noncentromeric circular plasmids containing various ARS elements, and extended linear yeast artificial chromosomes (YAC). These mutations led to an increase in the mitotic stability of some of the FGS tested and the disturbed maintenance of the others. Mutation srm1 imposed a stabilizing effect on the maintenance of various recombinant FGSs with ARS chromosomal elements. Mutation cdc28-srm destabilized the maintenance of only those recombinant FGS that shared full or detectable homology with sequences of the nuclear genome of the yeast cell.},\r\ncorrespondence_address1={Smirnova, M.E.; Institute of Molecular Genetics, Russian Academy of Sciences, Moscow 123182, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={7607435},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n UVS112—A gene involved in excision repair of yeast.\n \n \n \n \n\n\n \n Kozhina, T.; Kozhin, S.; Stepanova, V.; Yarovoy, B.; Donich, V.; Fedorova, I.; and Korolev, V.\n\n\n \n\n\n\n Yeast, 11(12): 1129-1138. 1995.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"UVS112—A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina19951129,\r\nauthor={Kozhina, T. and Kozhin, S. and Stepanova, V. and Yarovoy, B. and Donich, V. and Fedorova, I. and Korolev, V.},\r\ntitle={UVS112—A gene involved in excision repair of yeast},\r\njournal={Yeast},\r\nyear={1995},\r\nvolume={11},\r\nnumber={12},\r\npages={1129-1138},\r\ndoi={10.1002/yea.320111203},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0029097937&doi=10.1002%2fyea.320111203&partnerID=40&md5=8631dbbcbd08d72ea3297a663650de52},\r\naffiliation={Department of Molecular and Radiation Biology, Petersburg Institute of Nuclear Physics, Gatchina, 188350, Russian Federation; Petersburg Nuclear Physics Institute, Gatchina, 188350, Russian Federation},\r\nabstract={In this study we show that the previously described uvs112 (uvs12) mutation blocks one of the steps of the excision repair pathway. The properties of this mutation permit the assignment of the UVS112 gene to the RAD3 epistasis group. It was established that the uvs112 mutation caused a 2·5‐fold reduction in the number of recombinants produced by conversion and also significantly increased the frequency of mitotic crossing‐over in interplasmid recombination. Tetrad analysis placed the UVS112 gene on the left arm of chromosome IX, approximately 20 cM from HIS5. The analysis of mitotic recombination revealed that UVS112 lies between HIS6 and HIS5, and is an allele of the RAD25 gene. Copyright © 1995 John Wiley & Sons Ltd.},\r\nauthor_keywords={excision repair;  recombination;  Saccharomyces cerevisiae},\r\ncorrespondence_address1={Korolev, V.; Department of Molecular and Radiation Biology, Petersburg Institute of Nuclear Physics, Gatchina, 188350, Russian Federation},\r\nissn={0749503X},\r\npubmed_id={8619311},\r\nlanguage={English},\r\nabbrev_source_title={Yeast},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1994\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Cytogenetic analysis of the chromosome region containing the Drosophila radiosensitivity gene. II. The vitally important loci of the 44F-45C region of chromosome 2 [Tsitogeneticheskiǐ analiz uchastka khromosomy, soderzhashchego gen radiochuvstitel'nosti drozofily.II. Izuchenie zhiznenno vazhnykh lokus ov paiǒna 44F-45C khromosomy 2.].\n \n \n \n \n\n\n \n Konev, A.; Varentsova, E.; and Khromykh, I.\n\n\n \n\n\n\n Genetika, 30(2): 201-211. 1994.\n cited By 7\n\n\n\n
\n\n\n\n \n \n $\"Cytogenetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Konev1994201,\r\nauthor={Konev, A.I. and Varentsova, E.R. and Khromykh, I.M.},\r\ntitle={Cytogenetic analysis of the chromosome region containing the Drosophila radiosensitivity gene. II. The vitally important loci of the 44F-45C region of chromosome 2 [Tsitogeneticheskiǐ analiz uchastka khromosomy, soderzhashchego gen radiochuvstitel'nosti drozofily.II. Izuchenie zhiznenno vazhnykh lokus ov paiǒna 44F-45C khromosomy 2.]},\r\njournal={Genetika},\r\nyear={1994},\r\nvolume={30},\r\nnumber={2},\r\npages={201-211},\r\nnote={cited By 7},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0028376866&partnerID=40&md5=ba9b295555ab87859650e57d0bec14b3},\r\nabstract={Genetic content of 44F2-3; 4505-6 region of chromosome 2 characterized by an increased portion of heterochromatin rearrangements in comparison with other radiation-induced mutations, was studied. Eighteen complementation groups of lethal and viability reducing mutations were identified in 14 consecutive subregions of 44F-3; 4505-6 region using deletion and complementation analysis. Four additional complementation groups were formed only by rearrangements of heterochromatin. Location of heterochromatic aberrations does not coincide with hot spots of intralocus mutagenesis. Effective lethal period of mutations in 44F2-3; 45C5-6 region were analyzed. Mutations in 5 loci are lethal at the embryonic stage, strict lethal mutations of other genes lead to death at the larval stage. Mutations specifically changing scale and form of certain thorax bristles were identified in haplosensitive Notopleural locus which was not characterized earlier. Phenotypes of individuals homozygous for nonstrictly lethal alleles of vital loci of the region 44F-45C were described.},\r\ncorrespondence_address1={Konev, A.I.},\r\nissn={00166758},\r\npubmed_id={8045382},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Cytogenetic analysis of the chromosome region containing the Drosophila radiosensitivity gene. I. Cytogenetic mapping of the radiosensitivity gene [Tsitogeneticheskiǐ analiz uchastka khromosomy, soderzhashchego gen radiochuvstvitel'nosti drozofily.I. Tsitogeneticheskoe kartirovanie gena radiochuvstvitel'nosti.].\n \n \n \n \n\n\n \n Konev, A.; Varentsova, E.; Levina, V.; Sarantseva, S.; and Khromykh, I.\n\n\n \n\n\n\n Genetika, 30(2): 192-200. 1994.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"Cytogenetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Konev1994192,\r\nauthor={Konev, A.I. and Varentsova, E.R. and Levina, V.V. and Sarantseva, S.V. and Khromykh, I.M.},\r\ntitle={Cytogenetic analysis of the chromosome region containing the Drosophila radiosensitivity gene. I. Cytogenetic mapping of the radiosensitivity gene [Tsitogeneticheskiǐ analiz uchastka khromosomy, soderzhashchego gen radiochuvstvitel'nosti drozofily.I. Tsitogeneticheskoe kartirovanie gena radiochuvstvitel'nosti.]},\r\njournal={Genetika},\r\nyear={1994},\r\nvolume={30},\r\nnumber={2},\r\npages={192-200},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0028374035&partnerID=40&md5=d89e88e89f3c35f4fa2604d626ce6d68},\r\nabstract={Eleven deletions were obtained in the rad(2)201 radiosensitivity gene region and the 41-45B4 fragment duplication in the Y chromosome were made by using chromosome rearrangements that transfer the material of the 44F - 45D site of chromosome 2 in Drosophila melanogaster to heterochromatin. The locus rad(2)201 was mapped in thin band region 45B3 by using these rearrangements and 13 deletions isolated before. Analysis of the complementation of the rad(2)201G1 radiosensitivity mutation by lethals and chromosome rearrangements in the 44F2-3; 45C5-6 region did not reveal any lethal alleles of this gene. The translocation T(Y;2)G6 was isolated; in this translocation, the change of the rad(2)201 gene expression causes high sensitivity of rad(2)201G1/T(Y;2)G6 heterozygotes of the initiation of the radiation-induced morphoses, while the survival rate of individuals remains at the level of wild-type flies.},\r\ncorrespondence_address1={Konev, A.I.},\r\nissn={00166758},\r\npubmed_id={8045381},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

\n

\n \n 1993\n \n \n (3)\n \n \n

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\n \n \n

\n \n\n \n \n \n \n \n \n The XRS2 gene controls recombination repair in yeast.\n \n \n \n \n\n\n \n Chepurnaya, O.; Peshekhonov, V.; Kozhina, T.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 29(4): 571-580. 1993.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Chepurnaya1993571,\r\nauthor={Chepurnaya, O.V. and Peshekhonov, V.T. and Kozhina, T.N. and Korolev, V.G.},\r\ntitle={The XRS2 gene controls recombination repair in yeast},\r\njournal={Genetika},\r\nyear={1993},\r\nvolume={29},\r\nnumber={4},\r\npages={571-580},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027337495&partnerID=40&md5=94e4c57d1d91f14b5c122fcb100efa75},\r\naffiliation={St. Petersburg Inst. Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\ncorrespondence_address1={Chepurnaya, O.V.; St. Petersburg Inst. Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={8354468},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Rec41 - A new gene involved in the control of recombination in the yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Chepurnaya, O.; Kozhina, T.; Peshekhonov, V.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 29(2): 246-256. 1993.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Rec41$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Chepurnaya1993246,\r\nauthor={Chepurnaya, O.V. and Kozhina, T.N. and Peshekhonov, V.T. and Korolev, V.G.},\r\ntitle={Rec41 - A new gene involved in the control of recombination in the yeast Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={1993},\r\nvolume={29},\r\nnumber={2},\r\npages={246-256},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027253309&partnerID=40&md5=39f559cec1ced492f9705c16f73de6d4},\r\naffiliation={Petersburg Inst. of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\ncorrespondence_address1={Chepurnaya, O.V.; Petersburg Inst. of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={8486254},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic control of mitotic recombination in the yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Genetika, 29(2): 197-211. 1993.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1993197,\r\nauthor={Korolev, V.G.},\r\ntitle={Genetic control of mitotic recombination in the yeast Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={1993},\r\nvolume={29},\r\nnumber={2},\r\npages={197-211},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027195514&partnerID=40&md5=fb2d9985da1ab17cd75294cd7fa4fb34},\r\naffiliation={Petersburg Inst. of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\ncorrespondence_address1={Korolev, V.G.; Petersburg Inst. of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={8486250},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n

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\n

\n \n 1992\n \n \n (6)\n \n \n

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\n \n \n

\n \n\n \n \n \n \n \n \n Genetic control of meiotic recombination in yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Genetika, 28(11): 5-14. 1992.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev19925,\r\nauthor={Korolev, V.G.},\r\ntitle={Genetic control of meiotic recombination in yeast Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={1992},\r\nvolume={28},\r\nnumber={11},\r\npages={5-14},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026989233&partnerID=40&md5=74568af5ab1c6fc25e072ea6f63c5a3a},\r\naffiliation={St. Petersburg Inst. Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\ncorrespondence_address1={Korolev, V.G.; St. Petersburg Inst. Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={1286801},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n XRS2, a DNA repair gene of Saccharomyces cerevisiae, is needed for meiotic recombination.\n \n \n \n \n\n\n \n Ivanov, E.; Korolev, V.; and Fabre, F.\n\n\n \n\n\n\n Genetics, 132(3): 651-664. 1992.\n cited By 170\n\n\n\n
\n\n\n\n \n \n $\"XRS2,$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Ivanov1992651,\r\nauthor={Ivanov, E.L. and Korolev, V.G. and Fabre, F.},\r\ntitle={XRS2, a DNA repair gene of Saccharomyces cerevisiae, is needed for meiotic recombination},\r\njournal={Genetics},\r\nyear={1992},\r\nvolume={132},\r\nnumber={3},\r\npages={651-664},\r\nnote={cited By 170},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026759693&partnerID=40&md5=4e83afb9f3311fbb8c03b2e624634b52},\r\naffiliation={Rosenstiel Basic Med. Sci. Res. Ctr., Brandeis University, Waltham, MA 02254-9110, United States},\r\nabstract={The XRS2 gene of Saccharomyces cerevisiae has been previously identified as a DNA repair gene. In this communication, we show that XRS2 also encodes an essential meiotic function. Spore inviability of xrs2 strains is rescued by a spo13 mutation, but meiotic recombination (both gene conversion and crossing over) is highly depressed in spo13 xrs2 diploids. The xrs2 mutation suppresses spore inviability of a spo13 rad52 strain suggesting that XRS2 acts prior to RAD52 in the meiotic recombination pathway. In agreement with the genetic data, meiosis-specific double-strand breaks at the ARG4 meiotic recombination hotspot are not detected in xrs2 strains. Despite its effects on meiotic recombination, the xrs2 mutation does not prevent mitotic recombination events, including homologous integration of linear DNA, mating- type switching and radiation-induced gene conversion. Moreover, xrs2 strains display a mitotic hyper-rec phenotype. Haploid xrs2 cells fail to carry out G2-repair of gamma-induced lesions, whereas xrs2 diploids are able to perform some diploid-specific repair of these lesions. Meiotic and mitotic phenotypes of xrs2 cells are very similar to those of rad50 cells suggesting that XRS2 is involved in homologous recombination in a way analogous to that of RAD50.},\r\ncorrespondence_address1={Ivanov, E.L.; Rosenstiel Basic Med. Sci. Res. Ctr., Brandeis University, Waltham, MA 02254-9110, United States},\r\nissn={00166731},\r\ncoden={GENTA},\r\npubmed_id={1468624},\r\nlanguage={English},\r\nabbrev_source_title={GENETICS},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Comparative analysis of spontaneous mitotic recombination in [cir0] and [cir+] strains of the yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Pushnova, E.; Bulat, S.; and Korolev, V.\n\n\n \n\n\n\n Current Genetics, 22(4): 259-265. 1992.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Comparative$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Pushnova1992259,\r\nauthor={Pushnova, E.A. and Bulat, S.A. and Korolev, V.G.},\r\ntitle={Comparative analysis of spontaneous mitotic recombination in [cir0] and [cir+] strains of the yeast Saccharomyces cerevisiae},\r\njournal={Current Genetics},\r\nyear={1992},\r\nvolume={22},\r\nnumber={4},\r\npages={259-265},\r\ndoi={10.1007/BF00317918},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026640603&doi=10.1007%2fBF00317918&partnerID=40&md5=03c6fca7a529a7ddfc68b545e8e01a2f},\r\naffiliation={Laboratory of Genetics of Eukaryot, Department of Molecular and Radiation Biophysics, St. Petersburg Nuclear Physics Institute, Academy of Sciences of Russia, Gatchina, Russian Federation},\r\nabstract={The influence of the 2 μm plasmid on homologous recombination in the right arm of chromosome XV of the yeast Saccharomyces cerevisiae has been examined. No differences between spontaneous mitotic recombination rates in [cir0] and [cir+] derivatives of two yeast diploid tester strains were detected. In the course of analysis an unusually high coincident conversion frequency at ADE2, HIS3, and two RFLP loci adjacent to ADE2, was observed. The character of coincident homozygotization of linked markers argues for a "break-and-replicate" mechanism underlying the coincident conversion events. © 1992 Springer-Verlag.},\r\nauthor_keywords={2 μm plasmid;  Coincident conversion;  Mitotic recombination;  Yeast},\r\ncorrespondence_address1={Pushnova, E.A.; Laboratory of Genetics of Eukaryot, Department of Molecular and Radiation Biophysics, St. Petersburg Nuclear Physics Institute, Academy of Sciences of Russia, Gatchina, Russian Federation},\r\npublisher={Springer-Verlag},\r\nissn={01728083},\r\ncoden={CUGED},\r\npubmed_id={1356638},\r\nlanguage={English},\r\nabbrev_source_title={Curr Genet},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The system for analysis of yeast mutants deficient in genetic recombination process.\n \n \n \n \n\n\n \n Korolev, V.; Kozhina, T.; Kozhin, S.; Peshekhonov, V.; and Chepurnaya, O.\n\n\n \n\n\n\n Genetika, 28(7): 27-37. 1992.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev199227,\r\nauthor={Korolev, V.G. and Kozhina, T.N. and Kozhin, S.A. and Peshekhonov, V.T. and Chepurnaya, O.V.},\r\ntitle={The system for analysis of yeast mutants deficient in genetic recombination process},\r\njournal={Genetika},\r\nyear={1992},\r\nvolume={28},\r\nnumber={7},\r\npages={27-37},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026885079&partnerID=40&md5=d6f871c5f687c7c9050e2ca3499f6962},\r\naffiliation={Konstantinov St. Petersburg Inst., Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\ncorrespondence_address1={Korolev, V.G.; Konstantinov St. Petersburg Inst., Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={1427055},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Molecular-genetic analysis of radiation-induced mutation of the white gene, inserted in the 45D region of the second Drosophila melanogaster chromosome [Molekuliarno-geneticheskiǐ analiz radiatsionno indutsirovannykh mutatsiǐ gena white, insertirovannogo v raǐon 45D vtoroǐ khromosomy Drosophila melanogaster.].\n \n \n \n \n\n\n \n Anashchenko, V.; Sarantseva, S.; and Konev, A.\n\n\n \n\n\n\n Doklady Akademii nauk SSSR, 322(1): 161-165. 1992.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Molecular-genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Anashchenko1992161,\r\nauthor={Anashchenko, V.A. and Sarantseva, S.V. and Konev, A.I.},\r\ntitle={Molecular-genetic analysis of radiation-induced mutation of the white gene, inserted in the 45D region of the second Drosophila melanogaster chromosome [Molekuliarno-geneticheskiǐ analiz radiatsionno indutsirovannykh mutatsiǐ gena white, insertirovannogo v raǐon 45D vtoroǐ khromosomy Drosophila melanogaster.]},\r\njournal={Doklady Akademii nauk SSSR},\r\nyear={1992},\r\nvolume={322},\r\nnumber={1},\r\npages={161-165},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026464274&partnerID=40&md5=82b5fbb5b041a1263b5db977469ce34a},\r\ncorrespondence_address1={Anashchenko, V.A.},\r\nissn={00023264},\r\npubmed_id={1511665},\r\nlanguage={Russian},\r\nabbrev_source_title={Dokl Akad Nauk SSSR},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The gene HIM1 of the yeast Saccharomyces cerevisiae takes part in the correction of heteroduplex DNA.\n \n \n \n \n\n\n \n Gracheva, L.; Evstyukhina, T.; Kovaltsova, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 28(5): 56-65. 1992.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva199256,\r\nauthor={Gracheva, L.M. and Evstyukhina, T.A. and Kovaltsova, S.V. and Korolev, V.G.},\r\ntitle={The gene HIM1 of the yeast Saccharomyces cerevisiae takes part in the correction of heteroduplex DNA},\r\njournal={Genetika},\r\nyear={1992},\r\nvolume={28},\r\nnumber={5},\r\npages={56-65},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026856363&partnerID=40&md5=a35272bbf9d35f1bebc0925050f7c719},\r\naffiliation={Leningrad Inst. of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russia},\r\ncorrespondence_address1={Gracheva, L.M.; Leningrad Inst. of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russia},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={1639262},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1991\n \n \n (3)\n \n \n

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\n \n\n \n \n \n \n \n \n The cytogenetic study of the chromosomal region surrounding the radiosensitivity gene of Drosophila melanogaster. The influence of pericentrometric heterochromatin on mutagenesis in the 44-45 region of the chromosome 2.\n \n \n \n \n\n\n \n Konev Yu., A.; Varentsova, E.; and Khromykh Yu., M.\n\n\n \n\n\n\n Genetika, 27(4): 667-675. 1991.\n cited By 6\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{KonevYu.1991667,\r\nauthor={Konev Yu., A. and Varentsova, E.R. and Khromykh Yu., M.},\r\ntitle={The cytogenetic study of the chromosomal region surrounding the radiosensitivity gene of Drosophila melanogaster. The influence of pericentrometric heterochromatin on mutagenesis in the 44-45 region of the chromosome 2},\r\njournal={Genetika},\r\nyear={1991},\r\nvolume={27},\r\nnumber={4},\r\npages={667-675},\r\nnote={cited By 6},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025868815&partnerID=40&md5=b81589d4626d5065ffef789a3f98d770},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russia},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={1908803},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n A new system of selecting yeast mutants with disrupted genetic recombination processes [Novaia sistema otbora mutantaov drozhzheǐ s narusheniiami protsessov geneticheskoǐ rekombinatsii.].\n \n \n \n \n\n\n \n Kozhina, T.; Peshekhonov, V.; Chepurnaia, O.; and Korolev, V.\n\n\n \n\n\n\n Molekuliarnaia genetika, mikrobiologiia i virusologiia, (3): 13-16. 1991.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina199113,\r\nauthor={Kozhina, T.N. and Peshekhonov, V.T. and Chepurnaia, O.V. and Korolev, V.G.},\r\ntitle={A new system of selecting yeast mutants with disrupted genetic recombination processes [Novaia sistema otbora mutantaov drozhzheǐ s narusheniiami protsessov geneticheskoǐ rekombinatsii.]},\r\njournal={Molekuliarnaia genetika, mikrobiologiia i virusologiia},\r\nyear={1991},\r\nnumber={3},\r\npages={13-16},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026128665&partnerID=40&md5=4060148bcfe6672c5467bc73e75065b3},\r\nabstract={A new convenient system for isolation of the yeast mutants deficient in the genetical recombination is proposed. The chimeric plasmids constructed to carry the noncomplimenting mutant copy of the yeast ADE2 gene and different selectable yeast markers (LEU2 or TRP1 genes) are the basis for the system. Interplasmid intragenic recombination of ADE2 gene alleles in yeast cells transformed by two chimeric plasmids results in appearance of the secondary white prototrophic clones covering the primary red colony. The number of the clones reflects the recombination processes and is subject to an easy visual control. The proposed technique allows one to reveal both hypo and hyperrecombination mutants. Crossover or the gene conversion events can be distinguished by the simple genetical analysis of the secondary clones. The collection of mutants deficient in the genetical recombination has been obtained by the proposed technique.},\r\ncorrespondence_address1={Kozhina, T.N.},\r\nissn={02080613},\r\npubmed_id={1857368},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol Gen Mikrobiol Virusol},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Study of radiation mutagenesis in the 44-45 region of Drosophila melanogaster chromosome 2.\n \n \n \n \n\n\n \n Konev Yu., A.; Varentsova, E.; Sarantseva, S.; and Khromykh Yu., M.\n\n\n \n\n\n\n Genetika, 27(1): 77-87. 1991.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Study$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{KonevYu.199177,\r\nauthor={Konev Yu., A. and Varentsova, E.R. and Sarantseva, S.V. and Khromykh Yu., M.},\r\ntitle={Study of radiation mutagenesis in the 44-45 region of Drosophila melanogaster chromosome 2},\r\njournal={Genetika},\r\nyear={1991},\r\nvolume={27},\r\nnumber={1},\r\npages={77-87},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025846106&partnerID=40&md5=4b5503df12a885d9a4e6d73f92bd94fb},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russia},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={1903758},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1990\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Mapping of the XRS2 and HIM1 genes of Saccharomyces cerevisiae by the method based of the effect chromosomes destabilization.\n \n \n \n \n\n\n \n Kovaltsova, S.; Stepanova, V.; Yarovoi, B.; Korolev, V.; and Zakharov, I.\n\n\n \n\n\n\n Genetika, 26(9): 1667-1670. 1990.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Mapping$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kovaltsova19901667,\r\nauthor={Kovaltsova, S.V. and Stepanova, V.P. and Yarovoi, B.F. and Korolev, V.G. and Zakharov, I.A.},\r\ntitle={Mapping of the XRS2 and HIM1 genes of Saccharomyces cerevisiae by the method based of the effect chromosomes destabilization},\r\njournal={Genetika},\r\nyear={1990},\r\nvolume={26},\r\nnumber={9},\r\npages={1667-1670},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025481887&partnerID=40&md5=1ad2fae68c0a8a05ea8e1883f62734eb},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russia},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={2079209},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The start gene CDC28 and the genetic stability of yeast.\n \n \n \n \n\n\n \n Devin, A.; Prosvirova, T.; Peshekhonov, V.; Chepurnaya, O.; Smirnova, M.; Koltovaya, N.; Troitskaya, E.; and Arman, I.\n\n\n \n\n\n\n Yeast, 6(3): 231-243. 1990.\n cited By 27\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Devin1990231,\r\nauthor={Devin, A.B. and Prosvirova, T.Yu. and Peshekhonov, V.T. and Chepurnaya, O.V. and Smirnova, M.E. and Koltovaya, N.A. and Troitskaya, E.N. and Arman, I.P.},\r\ntitle={The start gene CDC28 and the genetic stability of yeast},\r\njournal={Yeast},\r\nyear={1990},\r\nvolume={6},\r\nnumber={3},\r\npages={231-243},\r\ndoi={10.1002/yea.320060308},\r\nnote={cited By 27},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025422641&doi=10.1002%2fyea.320060308&partnerID=40&md5=a3cb0b42d50e44a7c0a627da97a5750d},\r\naffiliation={Institute of Molecular Genetics, U.S.S.R. Academy of Sciences, Ademician Kurchatov Sq., Moscow, 123182; B. P. Konstantinov Institute of Nuclear Physics, U.S.S.R. Academy of Sciences, Gatchina, 188350; Joint Institute for Nuclear Research, Dubna, Moscow Region, 141980; A. N. Bach Institute of Biochemistry, U.S.S.R. Academy of Sciences, 33 Leninsky Prospekt, Moscow, 117071},\r\nabstract={The cdc28‐srm mutation in Saccheromyces cerevisiae decreases spontaneous and induced mitochondrial rhomutability and the mitotic stability of native chromosomes and recombinant circular minichromosomes. The effects of cdc28‐srm on the genetic stability of cells support the hypothesis that links cell cycle regulation in yeast to changes in chromatin organization dependent on the start gene CDC28 (Hayles and Nurse, 1986). Copyright © 1990 John Wiley & Sons Ltd.},\r\nauthor_keywords={CDC28 gene;  cell cycle regulation;  chromosome loss;  plasmid maintenance;  rho− mutation;  Saccharomyces cerevisiae},\r\ncorrespondence_address1={Devin, A.B.; Institute of Molecular Genetics, U.S.S.R. Academy of Sciences, Ademician Kurchatov Sq., Moscow, 123182},\r\nissn={0749503X},\r\npubmed_id={2190433},\r\nlanguage={English},\r\nabbrev_source_title={Yeast},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1989\n \n \n (4)\n \n \n

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\n \n\n \n \n \n \n \n \n Influence of him mutations characterized by enhanced induced mutagenesis on spontaneous mitotic gene conversion in the ADE2 gene of yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Kovaltsova, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 25(12): 2111-2120. 1989.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Influence$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kovaltsova19892111,\r\nauthor={Kovaltsova, S.V. and Korolev, V.G.},\r\ntitle={Influence of him mutations characterized by enhanced induced mutagenesis on spontaneous mitotic gene conversion in the ADE2 gene of yeast Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={1989},\r\nvolume={25},\r\nnumber={12},\r\npages={2111-2120},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024832885&partnerID=40&md5=b0e03f5a0bdd8cfe127ba37ec03ba9c3},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russia},\r\nabstract={We have studied the influence of him1, him2, and him3 and himX mutations on the frequency of spontaneous mitotic gene conversion in the yeast. Saccharomyces cerevisiae using the set of heteroallelic combinations in the ADE2 gene. Data obtained on the HIM/HIM, him/him homozygotes and HIM/him heterozygotes indicate that the him1 mutation is recessive with respect to conversion, whereas the him2, him3 and himX mutations are semidominant. Gene conversion was increased in the majority of heteroalleles of mutant diploids him1/him1. On the contrary, the him2, him3 and himX mutants have hypo-rec phenotypes on mitotic conversion. The him mutations do not affect some heteroalleles, moreover, for some heteroalleles, the effects of the him mutations was opposite. On the basis of the sum of genetical data and, particularly, of conversion event pattern in the him mutants, we suggest that him mutations analysed affect the repair pathway for mismatch correction.},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={2699460},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Restriction analysis of deletions and deletion mapping of point mutations in the ADE2 gene of Saccharomyces cerevisiae yeasts [Restriktsionnyǐ analiz deletsiǐ i deletsionnoe kartirovanie tochechnykh mutatsiǐ v gene ADE2 u drozhzheǐ Saccharomyces cerevisiae.].\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 25(8): 1356-1363. 1989.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Restriction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva19891356,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={Restriction analysis of deletions and deletion mapping of point mutations in the ADE2 gene of Saccharomyces cerevisiae yeasts [Restriktsionnyǐ analiz deletsiǐ i deletsionnoe kartirovanie tochechnykh mutatsiǐ v gene ADE2 u drozhzheǐ Saccharomyces cerevisiae.]},\r\njournal={Genetika},\r\nyear={1989},\r\nvolume={25},\r\nnumber={8},\r\npages={1356-1363},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024708816&partnerID=40&md5=08290c14aea87fbff8c2fad8fc7719d3},\r\nabstract={The method of restriction analysis has been used to study the length of 10 deletion mutations in ADE2 locus of Saccharomyces cerevisiae. We showed that 7 deletions overlapped the whole transcribed region of the gene ADE2, while 3 deletions have one of the ends situated in this region. Four controlled sites were fixed on the genetic map of ADE2 locus, based on these results. Deletion mapping of great number of point mutations demonstrated non-random distribution of mutations of different types on the map of ADE2 locus.},\r\ncorrespondence_address1={Gracheva, L.M.},\r\nissn={00166758},\r\npubmed_id={2684746},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutagenesis in cloned yeast genes. The effect of mutation rad2 on the frequency of gene mutation in plasmid and chromosome [Mutagenez na klonirovannykh drozhzhevykh genakh. Vliianie mutatsii rad2 na chastotu mutirovaniia gena v sostave plazmidy i khromosomy.].\n \n \n \n \n\n\n \n Fedorova, I.; Korolev, V.; and Gracheva, L.\n\n\n \n\n\n\n Genetika, 25(5): 937-940. 1989.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Mutagenesis$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Fedorova1989937,\r\nauthor={Fedorova, I.V. and Korolev, V.G. and Gracheva, L.M.},\r\ntitle={Mutagenesis in cloned yeast genes. The effect of mutation rad2 on the frequency of gene mutation in plasmid and chromosome [Mutagenez na klonirovannykh drozhzhevykh genakh. Vliianie mutatsii rad2 na chastotu mutirovaniia gena v sostave plazmidy i khromosomy.]},\r\njournal={Genetika},\r\nyear={1989},\r\nvolume={25},\r\nnumber={5},\r\npages={937-940},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024670867&partnerID=40&md5=cc1ff4759f45a47e6252dfcf67e55983},\r\nabstract={The influence of rad2 mutation blocking incision of pyrimidine dimers on frequency of UV-light and 6-hydroxylaminopurine (6-GAP)-induced adenine-independent revertants was studied in the strains of Saccharomyces cerevisiae containing the same mutant allele of gene ADE2 in episomic plasmid and in chromosome. It was shown that the strains carrying the ade2 mutation in chromosome and in plasmid did not differ in sensitivity to lethal action of UV-light and 6-GAP. However, in the plasmid rad2 strain reversions were induced by UV-light more frequently (approximately 100 times), as compared to the chromosome strain. We observed no significant differences between reversion frequencies in plasmid and chromosome RAD strains. The tendency to enhanced 6-GAP-induced mutagenesis, less sharply expressed, was observed in the chromosome rad2 strain, as compared to the plasmid one. However, the plasmid RAD strain was characteristic of higher reversion frequency induced by 6-GAP, as compared to the chromosome strain. The possible mechanisms of these phenomena are discussed.},\r\ncorrespondence_address1={Fedorova, I.V.},\r\nissn={00166758},\r\npubmed_id={2663640},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Saccharomyces cerevisiae mutants with enhanced induced mutation and altered mitotic gene conversion.\n \n \n \n \n\n\n \n Ivanov, E.; Kovaltzova, S.; and Korolev, V.\n\n\n \n\n\n\n Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 213(2): 105-115. 1989.\n cited By 16\n\n\n\n
\n\n\n\n \n \n $\"Saccharomyces$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Ivanov1989105,\r\nauthor={Ivanov, E.L. and Kovaltzova, S.V. and Korolev, V.G.},\r\ntitle={Saccharomyces cerevisiae mutants with enhanced induced mutation and altered mitotic gene conversion},\r\njournal={Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis},\r\nyear={1989},\r\nvolume={213},\r\nnumber={2},\r\npages={105-115},\r\ndoi={10.1016/0027-5107(89)90141-3},\r\nnote={cited By 16},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024359631&doi=10.1016%2f0027-5107%2889%2990141-3&partnerID=40&md5=f19c7ea2b5e5891bb6ffaf130ace757b},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences, the U.S.S.R., 188350 Gatchina, Russian Federation},\r\nabstract={We have developed a method to isolate yeast (Saccharomyces cerevisiae) mutants with enhanced induced mutagenesis based on nitrous acid-induced reversion of the ade2-42 allele. Six mutants have been isolated and designated him (high induced mutagenesis), and 4 of them were studied in more detail. The him mutants displayed enhanced reversion of the ade2-42 allele, either spontaneous or induced by nitrous acid, UV light, and the base analog 6-N-hydroxylaminopurine, but not by γ-irradiation. It is worth noting that the him mutants turned out not to be sensitive to the lethal effects of the mutagens used. The enhancement in mutation induced by nitrous acid, UV light, and 6-N-hydroxylaminopurine has been confirmed in a forward-mutation assay (induction of mutations in the ADE1, ADE2 genes). The latter agent revealed the most apparent differences between the him mutants and the wild-type strain and was, therefore, chosen for the genetic analysis of mutants. him mutations analyzed behaved as a single Mendelian trait; complementation tests indicated 3 complementation groups (HIM1, HIM2, and HIm3), each containing 1 mutant allele. Uracil-DNA glycosylase activity was determined in crude cell extracts, and no significant differences between the wild-type and him strains detected. Spontaneous mitotic gene conversion at the ADE2 locus is altered in him1 strains, either increased or decreased, depending on the particular heteroallelic combination. Genetic evidence strongly suggests him mutations to be involved in a process of mismatch correction of molecular heteroduplexes. © 1989.},\r\nauthor_keywords={Enhanced mutagenesis;  Mitotic gene conversion;  S. cerevisiae},\r\ncorrespondence_address1={Ivanov, E.L.; B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences, the U.S.S.R., 188350 Gatchina, Russian Federation},\r\nissn={00275107},\r\ncoden={MRFME},\r\npubmed_id={2668746},\r\nlanguage={English},\r\nabbrev_source_title={Mutat. Res. Fundam. Mol. Mech. Mutagen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1988\n \n \n (4)\n \n \n

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\n \n\n \n \n \n \n \n \n Genetic analysis of mitochondrial rho-mutability in Saccharomyces yeasts. VI. Quantitative characteristics of the effect of mutation srm5 on the mitochondrial stability of natural and recombinant genetic structures [Geneticheskiǐ analiz mitokhondrial'noǐ rho-mutabil'nosti u drozhzheǐ sakharomitsetov. Soobshchenie VI. Kolichestvennye kharakteristiki vliianiia mutatsii srm5 na mitoticheskuiu stabil'nost' prirodnykh i rekombinantnykh geneticheskikh struktur.].\n \n \n \n \n\n\n \n Koltovaia, N.; Peshekhonov, V.; Prosvirov, T.; Smirnova, M.; and Chepurnaia, O.\n\n\n \n\n\n\n Genetika, 24(10): 1761-1767. 1988.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Koltovaia19881761,\r\nauthor={Koltovaia, N.A. and Peshekhonov, V.T. and Prosvirov, T.I. and Smirnova, M.E. and Chepurnaia, O.V.},\r\ntitle={Genetic analysis of mitochondrial rho-mutability in Saccharomyces yeasts. VI. Quantitative characteristics of the effect of mutation srm5 on the mitochondrial stability of natural and recombinant genetic structures [Geneticheskiǐ analiz mitokhondrial'noǐ rho-mutabil'nosti u drozhzheǐ sakharomitsetov. Soobshchenie VI. Kolichestvennye kharakteristiki vliianiia mutatsii srm5 na mitoticheskuiu stabil'nost' prirodnykh i rekombinantnykh geneticheskikh struktur.]},\r\njournal={Genetika},\r\nyear={1988},\r\nvolume={24},\r\nnumber={10},\r\npages={1761-1767},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024103299&partnerID=40&md5=9540b2992ae8ca524d8ae63ce4bfe614},\r\nabstract={The srm5 mutation diminishes the spontaneous rho- mutation rate by an order of magnitude. Frequency of rho- mutations is 500 times lower in homozygous cultures, as compared with those of normal SRM+/SRM+ diploids. The rate of spontaneous loss of extra chromosome IV is about 25 times higher in srm5 disomes, as compared with SRM+ ones. Haploid srm1 srm5 transformants loose recombinant circular minichromosomes spontaneously about 4 times more frequently than srm1SRM5 cells. The data presented suggest that general control of mitotic stability of different (mitochondrial and nuclear, nuclear as well as recombinant) genetic structures operates in Sacch. cerevisiae. Autonomously replicating sequences (ARS elements) seem to be involved in this mechanism.},\r\ncorrespondence_address1={Koltovaia, N.A.},\r\nissn={00166758},\r\npubmed_id={3069578},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutagenesis on cloned yeast genes. The mutation of the yeast gene comprising the plasmid and chromosome [Mutagenez na klonirovannykh genakh drozhzheǐ. Mutirovanie gena drozhzheǐ v sostave plazmidy i khromosomy.].\n \n \n \n \n\n\n \n Gracheva, L.; Kasinova, G.; Korolev, V.; and Fedorova, I.\n\n\n \n\n\n\n Genetika, 24(7): 1178-1186. 1988.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Mutagenesis$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva19881178,\r\nauthor={Gracheva, L.M. and Kasinova, G.V. and Korolev, V.G. and Fedorova, I.V.},\r\ntitle={Mutagenesis on cloned yeast genes. The mutation of the yeast gene comprising the plasmid and chromosome [Mutagenez na klonirovannykh genakh drozhzheǐ. Mutirovanie gena drozhzheǐ v sostave plazmidy i khromosomy.]},\r\njournal={Genetika},\r\nyear={1988},\r\nvolume={24},\r\nnumber={7},\r\npages={1178-1186},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024043112&partnerID=40&md5=bbf6d0a0b4b317984ac297c8f27f2b59},\r\nabstract={The cells of Saccharomyces cerevisiae were transformed by plasmid pYG-007 treated in vitro with o-methylhydroxylamine. The plasmid consists of a portion of the bacterial plasmid with genes of resistance to ampicillin, chloramphenicol and tetracycline, 2 mkm yeast DNA and yeast genes ADE2 and LEU2. The collection of mutants containing a mutant allele of ADE2 gene within the plasmid was obtained. Interallelic complementation and that induced by suppression were studied in these ade 2 mutants. It was shown that all these induced ade 2 mutations were base-pair substitutions. Using the mechanism of conversion we managed to transfer the plasmid ade 2 mutations into the chromosome. Three pairs of strains carrying similar mutation in plasmid and chromosome were created. Analysis of frequency of reversions induced by UV-light and hydroxylaminopurine in the mutant ade2 locus comprised in the plasmid and chromosome showed that the former induced reversions in plasmid alleles less effectively than the latter.},\r\ncorrespondence_address1={Gracheva, L.M.},\r\nissn={00166758},\r\npubmed_id={3053331},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic control of plasmid recombination in the cotransformation of Saccharomyces cerevisiae: the role of RAD52 and FLP genes [Geneticheskiǐ kontrol' rekombinatsii plazmid pri kotransformatsii Saccharomyces cerevisiae: rol' genov RAD52 i FLP.].\n \n \n \n \n\n\n \n Kozhina, T.; Peshekhonov, V.; and Chepurnaia, O.\n\n\n \n\n\n\n Genetika, 24(6): 993-997. 1988.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Kozhina1988993,\r\nauthor={Kozhina, T.N. and Peshekhonov, V.T. and Chepurnaia, O.V.},\r\ntitle={Genetic control of plasmid recombination in the cotransformation of Saccharomyces cerevisiae: the role of RAD52 and FLP genes [Geneticheskiǐ kontrol' rekombinatsii plazmid pri kotransformatsii Saccharomyces cerevisiae: rol' genov RAD52 i FLP.]},\r\njournal={Genetika},\r\nyear={1988},\r\nvolume={24},\r\nnumber={6},\r\npages={993-997},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024023276&partnerID=40&md5=a5c3ef17149850f60165b5125b75f70f},\r\nabstract={In our earlier works we observed high frequency of recombination between two chimeric plasmids of different types, when they were introduced into yeast cells via cotransformation. Incapability of one of these plasmids to replicate autonomously in yeast cell is the necessary condition for such recombination. The high efficiency of this process point to the differences between interplasmid recombination and other types of yeast recombination. In this work, we studied the participation of two genes in the control of interplasmid exchanges. These are RAD52 responsible for normal processes of meiotic and mitotic recombination and highly specific gene FLP located on 2 mkm DNA which specifies site-specific recombination in the region of inverted sequences of this plasmid. The mutation rad52 in the recipient strain was shown to sharply decrease the efficiency of recombination between integrative and episome plasmids during cotransformation. The absence of FLP gene in the recipient strain (cirO) has no influence on this process.},\r\ncorrespondence_address1={Kozhina, T.N.},\r\nissn={00166758},\r\npubmed_id={3049236},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic effects of decay of radionuclides, products of nuclear fission, in Saccharomyces cerevisiae yeast cells. The lethal effect of decay of 89Sr incorporated in cells of different ploidy and radiosensitivity.\n \n \n \n \n\n\n \n Korolev, V.; and Gracheva, L.\n\n\n \n\n\n\n Radiobiologiya, 28(1): 134-137. 1988.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev1988134,\r\nauthor={Korolev, V.G. and Gracheva, L.M.},\r\ntitle={Genetic effects of decay of radionuclides, products of nuclear fission, in Saccharomyces cerevisiae yeast cells. The lethal effect of decay of 89Sr incorporated in cells of different ploidy and radiosensitivity},\r\njournal={Radiobiologiya},\r\nyear={1988},\r\nvolume={28},\r\nnumber={1},\r\npages={134-137},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023868552&partnerID=40&md5=7b3ee235235afc55b2dc80386eda6aae},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, USSR Academy of Sciences, Gatchina},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={3278334},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1987\n \n \n (4)\n \n \n

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\n \n\n \n \n \n \n \n \n The srm mutations which reduce mitochondrial rho-mutability affect the stability of ring minichromosomes in Saccharomyces cerevisiae [Mutatsii srm, snizhaiushchie mitokhondrial'nuiu rho-mutabil'nost', vliiaiut na stabil'nost' kol'tsevykh minikhromosom u Saccharomyces cerevisiae.].\n \n \n \n \n\n\n \n Peshekhonov, V.; Chepurnaia, O.; and Devin, A.\n\n\n \n\n\n\n Doklady Akademii nauk SSSR, 295(6): 1476-1479. 1987.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Peshekhonov19871476,\r\nauthor={Peshekhonov, V.T. and Chepurnaia, O.V. and Devin, A.B.},\r\ntitle={The srm mutations which reduce mitochondrial rho-mutability affect the stability of ring minichromosomes in Saccharomyces cerevisiae [Mutatsii srm, snizhaiushchie mitokhondrial'nuiu rho-mutabil'nost', vliiaiut na stabil'nost' kol'tsevykh minikhromosom u Saccharomyces cerevisiae.]},\r\njournal={Doklady Akademii nauk SSSR},\r\nyear={1987},\r\nvolume={295},\r\nnumber={6},\r\npages={1476-1479},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023473874&partnerID=40&md5=41187c9c9e707f543a4c5b7616424cb5},\r\ncorrespondence_address1={Peshekhonov, V.T.},\r\nissn={00023264},\r\npubmed_id={3315532},\r\nlanguage={Russian},\r\nabbrev_source_title={Dokl Akad Nauk SSSR},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutants of the yeast Saccharomyces cerevisiae characterized by enhanced induced mutagenesis. III. Effect of the him mutation on the effectiveness and specificity of UF-induced mutagenesis [Mutanty drozhzheǐ Saccharomyces cerevisiae, kharakterizuiushchiesia povyshennym indutsirovannym mutagenezom. Soobshchenie III. Vliianie mutatsii him na éffektivnost' i spetsifichnost' UF-indutsirovannogo mutageneza.].\n \n \n \n \n\n\n \n Ivanov, E.; Koval'tsova, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 23(9): 1555-1563. 1987.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"Mutants$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Ivanov19871555,\r\nauthor={Ivanov, E.L. and Koval'tsova, S.V. and Korolev, V.G.},\r\ntitle={Mutants of the yeast Saccharomyces cerevisiae characterized by enhanced induced mutagenesis. III. Effect of the him mutation on the effectiveness and specificity of UF-induced mutagenesis [Mutanty drozhzheǐ Saccharomyces cerevisiae, kharakterizuiushchiesia povyshennym indutsirovannym mutagenezom. Soobshchenie III. Vliianie mutatsii him na éffektivnost' i spetsifichnost' UF-indutsirovannogo mutageneza.]},\r\njournal={Genetika},\r\nyear={1987},\r\nvolume={23},\r\nnumber={9},\r\npages={1555-1563},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023405359&partnerID=40&md5=f58bbca37e967e05849ca9a563792caa},\r\nabstract={We have studied the influence of him1-1, him2-1, him3-1 and himX mutations on induction frequency and specificity of UV-induced adenine-dependent mutations in the yeast Saccharomyces cerevisiae. Him mutations do not render haploid cells more sensitive to the lethal action of UV-light; however, in him strains adenine-dependent mutations (ade1, ade2) were induced more frequently (1.5--2-fold), as compared to the HIM strain. An analysis of the molecular nature of ade2 mutants revealed that him1-1, him2-1 and himX mutations increase specifically the yield of transitions (AT----GC and GC----AT), whereas in the him3-1 strain the yield of transversions was enhanced as well. We suggest him mutations analysed to affect specific repair pathway for mismatch correction.},\r\ncorrespondence_address1={Ivanov, E.L.},\r\nissn={00166758},\r\npubmed_id={3319773},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Saccharomyces cerevisiae mutants characterized by increased induced mutagenesis. II. Genetic analysis of mutants [Mutanty drozhzheǐ Saccharomyces cerevisiae, kharakterizuiushchiesia povyshennym indutsirovannym mutagenezom. Soobshchenie II. Geneticheskiǐ analiz mutantov.].\n \n \n \n \n\n\n \n Ivanov, E.; Bulat, S.; Korolev, V.; and Koval'tsova, S.\n\n\n \n\n\n\n Genetika, 23(8): 1383-1389. 1987.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Saccharomyces$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Ivanov19871383,\r\nauthor={Ivanov, E.L. and Bulat, S.A. and Korolev, V.G. and Koval'tsova, S.V.},\r\ntitle={Saccharomyces cerevisiae mutants characterized by increased induced mutagenesis. II. Genetic analysis of mutants [Mutanty drozhzheǐ Saccharomyces cerevisiae, kharakterizuiushchiesia povyshennym indutsirovannym mutagenezom. Soobshchenie II. Geneticheskiǐ analiz mutantov.]},\r\njournal={Genetika},\r\nyear={1987},\r\nvolume={23},\r\nnumber={8},\r\npages={1383-1389},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023390937&partnerID=40&md5=0ba8da97a6b9b62d21d085d7af699537},\r\nabstract={Induction of forward adenine-dependent (Ade+----Ade-) mutations by HAP was used to analyse genetically yeast mutants with enhanced induced mutagenesis. Three mutations studied in detail segregated as a single mendelian trait and composed independent complementation groups (HIM1, HIM2, HIM3). the him1-1 mutation was centromere-linked, the him3-1 and him2-1 mutations being not. All three mutations did not show any cross-linkage. Uracil-DNA glycosylase activity was determined in crude cell extract from wild type strain and him mutants; no detectable differences were observed.},\r\ncorrespondence_address1={Ivanov, E.L.},\r\nissn={00166758},\r\npubmed_id={3311878},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutants of Saccharomyces cerevisiae characterized by increased level of induced mutagenesis. I. Isolation and preliminary characterization of mutants [Mutanty drozhzheǐ Saccharomyces cerevisiae, kharakterizuiushchiesia povyshennym indutsirovannym mutagenezom. Soobshchenie I. Vydelenie mutantov i ikh predvaritel'noe izuchenie.].\n \n \n \n \n\n\n \n Ivanov, E.; Koval'tsova, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 23(5): 784-792. 1987.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"Mutants$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Ivanov1987784,\r\nauthor={Ivanov, E.L. and Koval'tsova, S.V. and Korolev, V.G.},\r\ntitle={Mutants of Saccharomyces cerevisiae characterized by increased level of induced mutagenesis. I. Isolation and preliminary characterization of mutants [Mutanty drozhzheǐ Saccharomyces cerevisiae, kharakterizuiushchiesia povyshennym indutsirovannym mutagenezom. Soobshchenie I. Vydelenie mutantov i ikh predvaritel'noe izuchenie.]},\r\njournal={Genetika},\r\nyear={1987},\r\nvolume={23},\r\nnumber={5},\r\npages={784-792},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023340493&partnerID=40&md5=b39e4938e4aab904f44a0a71fb0d472e},\r\nabstract={6 mutants with enhanced nitrous acid-induced reversibility of the ade2-42 allele were isolated and designated hm (high mutagenesis). Apart from sensitivity to the mutagenic exposure to nitrous acid, hm mutants were also spontaneous mutators and hypermutable under the action of UV-light and 6-N-hydroxyaminopurine. All these effects were detected not only when analysing reversibility of the ade2-42 allele, but also when scoring forward mutations in the ADE1, ADF2 genes. Gamma-mutagenesis, however, was not affected by hm mutations.},\r\ncorrespondence_address1={Ivanov, E.L.},\r\nissn={00166758},\r\npubmed_id={3305160},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1986\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n The rad2 mutation effects the molecular nature of UV and acridine-mustard-induced mutations in the ADE2 gene of Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Ivanov, E.; Kovaltzova, S.; Kassinova, G.; Gracheva, L.; Korolev, V.; and Zakharov, I.\n\n\n \n\n\n\n Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 160(3): 207-214. 1986.\n cited By 7\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Ivanov1986207,\r\nauthor={Ivanov, E.L. and Kovaltzova, S.V. and Kassinova, G.V. and Gracheva, L.M. and Korolev, V.G. and Zakharov, I.A.},\r\ntitle={The rad2 mutation effects the molecular nature of UV and acridine-mustard-induced mutations in the ADE2 gene of Saccharomyces cerevisiae},\r\njournal={Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis},\r\nyear={1986},\r\nvolume={160},\r\nnumber={3},\r\npages={207-214},\r\ndoi={10.1016/0027-5107(86)90129-6},\r\nnote={cited By 7},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022517856&doi=10.1016%2f0027-5107%2886%2990129-6&partnerID=40&md5=342bb97cd90817ecf00c5af057a374f3},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences, the U.S.S.R., Gatchina, 188350, Russian Federation},\r\nabstract={We have studied the molecular nature of ade2 mutations induced by UV light and bifunctional acridine-mustard (BAM) in wild-type (RAD) and in excision-deficient (rad2) strains of the yeast, Saccharomyces cerevisiae. In the RAD strain, UV causes 45% GC → AT transitions among all mutations; in the rad2 strain this value is 77%. BAM was shown to be highly specific for frameshift mutagenesis: 60% frameshifts in the RAD strain, and as many as 84% frameshifts in the rad2 strain were induced. Therefore, the rad2 mutation affects the specificity of UV- and BAM-induced mutagenesis in yeast. Experimental data agree with the view that the majority of mutations in the RAD strain are induced by a prereplicative mechanism, whereas mutations in the RAD strain are induced by a prereplicative mechanism, whereas mutations in the rad2 strain are predominantly postreplicative events. Our results also suggest that: (1) cytosine-containing photoproducts are the substances responsible for major premutational damage to DNA; (2) a fraction of the mutations may arise in the course of excision repair of UV photoproducts. © 1986.},\r\ncorrespondence_address1={Ivanov, E.L.; B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences, the U.S.S.R., Gatchina, 188350, Russian Federation},\r\nissn={00275107},\r\ncoden={MRFME},\r\npubmed_id={2421157},\r\nlanguage={English},\r\nabbrev_source_title={Mutat. Res. Fundam. Mol. Mech. Mutagen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1985\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Cloning of a yeast gene \"in vivo\" and its transfer as a part of an autonomously replicating unit: gene seduction.\n \n \n \n \n\n\n \n Bulat, S.; Peshekhonov, V.; Chepurnaya, O.; and Zakharov, I.\n\n\n \n\n\n\n Current Genetics, 9(2): 119-121. 1985.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Cloning$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Bulat1985119,\r\nauthor={Bulat, S.A. and Peshekhonov, V.T. and Chepurnaya, O.V. and Zakharov, I.A.},\r\ntitle={Cloning of a yeast gene "in vivo" and its transfer as a part of an autonomously replicating unit: gene seduction},\r\njournal={Current Genetics},\r\nyear={1985},\r\nvolume={9},\r\nnumber={2},\r\npages={119-121},\r\ndoi={10.1007/BF00436958},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021912460&doi=10.1007%2fBF00436958&partnerID=40&md5=ae8f6b33cfcdce1a84aee6c953be484b},\r\naffiliation={Laboratory of Molecular and Radiation Biophysics, B. P. Konstantinov Leningrad Institut of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russia},\r\nabstract={Yeast diploids containing a chromosomally integrated episomal plasmid manifest the mitotic instability of the chromosomes with the plasmid. Probably as a results of the destabilization integrated plasmid may be excised out of the chromosome. It was found that the rescue of the plasmid may be irregular, with the taking up of adjacent chromosomal gene. Using an integrant with the plasmid integrated into chromosome I very near the ADE1 locus we cloned this gene "in vivo" by selecting rescued plasmid marker LEU2. The new plasmid has retained the LEU2 gene and the capacity to replicate autonomously. This plasmid was used to transfer the cloned ADEI gene from one cell to another by transformation and from one resident chromosome to another by integration. The phenomenon of irregular excision of an integrated episomal plasmid together with linked chromosomal gene(s) and transfer to other chromosomes or cells we propose to term Seduction. © 1985 Springer-Verlag.},\r\nauthor_keywords={Chromosomal integration;  Episomal plasmid;  Gene seduction;  Plasmid rescue},\r\ncorrespondence_address1={Bulat, S.A.; Laboratory of Molecular and Radiation Biophysics, B. P. Konstantinov Leningrad Institut of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russia},\r\npublisher={Springer-Verlag},\r\nissn={01728083},\r\ncoden={CUGED},\r\nlanguage={English},\r\nabbrev_source_title={Curr Genet},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutagenic effect and mutation spectrum induced by 3H decay in the 8th position of DNA purine bases in Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Korolev, V.; and Ivanov, E.\n\n\n \n\n\n\n Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 149(3): 359-364. 1985.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"Mutagenic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev1985359,\r\nauthor={Korolev, V.G. and Ivanov, E.L.},\r\ntitle={Mutagenic effect and mutation spectrum induced by 3H decay in the 8th position of DNA purine bases in Saccharomyces cerevisiae},\r\njournal={Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis},\r\nyear={1985},\r\nvolume={149},\r\nnumber={3},\r\npages={359-364},\r\ndoi={10.1016/0027-5107(85)90152-6},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021929158&doi=10.1016%2f0027-5107%2885%2990152-6&partnerID=40&md5=da911558b82f2e4078fc481cf0c1a92b},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences, the U.S.S.R., Gatchina, 188350, Russian Federation},\r\nabstract={Lethal and mutagenic effects and the mutation spectrum induced by 3H decay in the 8th position of adenine and guanine in yeast DNA have been studied. For haploid cells labelled with [8-3H]deoxyadenosinemonophosphate (8-3H-A) and [8-3H]deoxyguanosinemonophosphate (8-3H-G), the lethal efficiencies were determined as (3.0 ± 0.8) · 10-3 decay-1 and (3.8 ± 0.6) · 10-3 decay-1, respectively, and the mutagenic efficiencies as (5.7 ± 1.1) · 10-8 decay-1 and (8.7 ± 1.4) · 10-8 decay-1, respectively. The lethal effect of [8-3H]purines may be explained as being due to internal β-irradiation. In contrast, the local effect of 3H-transmutation was twice as mutagenic as β-irradiation when the induction of forward gene mutations was examined. Within the spectrum of mutations induced by 8-3H-G, a preference for GC → AT transitions was observed. © 1985.},\r\ncorrespondence_address1={Korolev, V.G.; B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences, the U.S.S.R., Gatchina, 188350, Russian Federation},\r\nissn={00275107},\r\ncoden={MRFME},\r\npubmed_id={3887147},\r\nlanguage={English},\r\nabbrev_source_title={Mutat. Res. Fundam. Mol. Mech. Mutagen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1984\n \n \n (5)\n \n \n

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\n \n \n

\n \n\n \n \n \n \n \n \n In vivo cloning of a yeast gene and its transfer with an autonomously replicating element: The gene seduction.\n \n \n \n \n\n\n \n Bulat, S.; Peshekhonov, V.; Chepurnaya, O.; and Zakharov, I.\n\n\n \n\n\n\n Doklady Biological Sciences, 277(1-6): 461-464. 1984.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"In$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Bulat1984461,\r\nauthor={Bulat, S.A. and Peshekhonov, V.T. and Chepurnaya, O.V. and Zakharov, I.A.},\r\ntitle={In vivo cloning of a yeast gene and its transfer with an autonomously replicating element: The gene seduction},\r\njournal={Doklady Biological Sciences},\r\nyear={1984},\r\nvolume={277},\r\nnumber={1-6},\r\npages={461-464},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021733258&partnerID=40&md5=be079d69ea80be916a03661951eb31ee},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Leningrad, Russia},\r\nissn={00124966},\r\ncoden={DKBSA},\r\nlanguage={English},\r\nabbrev_source_title={DOKL. BIOL. SCI.},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic consequences of decay via the scheme of radionuclide electron capture in a yeast cell [Geneticheskie posledstviia raspada po skheme élektronnogo zakhvata radionuklidov v kletke drozhzheǐ.].\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 20(8): 1264-1269. 1984.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Gracheva19841264,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={Genetic consequences of decay via the scheme of radionuclide electron capture in a yeast cell [Geneticheskie posledstviia raspada po skheme élektronnogo zakhvata radionuklidov v kletke drozhzheǐ.]},\r\njournal={Genetika},\r\nyear={1984},\r\nvolume={20},\r\nnumber={8},\r\npages={1264-1269},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021475409&partnerID=40&md5=1df3b5a6c79e1f8901f701ff9bc6081c},\r\nabstract={The lethal, mutagenic effects and the nature of mutations induced by decay of radionuclei incorporated into yeast cell were studied by K-cupture. The efficiency of inactivation per decay in a cell has been shown to be (2.23 +/- 0,70) X 10(-3) and (0.90 +/- 0.47) X 10(-3) for 54Mn and 85Sr, respectively. The efficiency of mutation production in ADE1 and ADE2 genes per decay is (1.25 +/- 0.57) X 10(-8) and (1.8 +/- 0.3) X 10(-9) for 54Mn and 85Sr, respectively, the lethal and mutagenic efficiency of 7Be being about zero. The relative mutagenic efficiency (RME), demonstrated as a ratio of the mutagenic efficiency of a mutagen to that or gamma-rays at the equal value of survival makes 0.25 for 54Mn and 0.1 for 85Sr. A frequency of the induced frameshift mutations was increased, in comparison with the frequency of mutations induced by clear beta-decay of radionuclei.},\r\ncorrespondence_address1={Gracheva, L.M.},\r\nissn={00166758},\r\npubmed_id={6386601},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Imitation of radiation-induced damages to DNA with a radionuclide incorporated into polynucleotides.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Radiobiologiya, 24(6): 728-738. 1984.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Imitation$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1984728,\r\nauthor={Korolev, V.G.},\r\ntitle={Imitation of radiation-induced damages to DNA with a radionuclide incorporated into polynucleotides},\r\njournal={Radiobiologiya},\r\nyear={1984},\r\nvolume={24},\r\nnumber={6},\r\npages={728-738},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021527530&partnerID=40&md5=e351231a1547d028d73da4e16f4d7015},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, USSR Academy of Sciences, Gatchina},\r\nabstract={Because of a great variety and different reparability of radiation-induced DNA lesions it is difficult to evaluate the radiobiological significance of certain individual alterations. It is suggested that the radionuclides incorporated into DNA can be used to imitate different types of radiation damages to DNA. Both qualitative and quantitative aspects of the problem are discussed.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={6393202},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Simulation of the effects of radiation-induced DNA lesions and genetic hazards from radioactive decay.\n \n \n \n \n\n\n \n Korolev, V.; and Ivanov, E.\n\n\n \n\n\n\n Radiobiologiya, 24(5): 659-662. 1984.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Simulation$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1984659,\r\nauthor={Korolev, V.G. and Ivanov, E.L.},\r\ntitle={Simulation of the effects of radiation-induced DNA lesions and genetic hazards from radioactive decay},\r\njournal={Radiobiologiya},\r\nyear={1984},\r\nvolume={24},\r\nnumber={5},\r\npages={659-662},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021488962&partnerID=40&md5=a460e0f381125afb00b6270013dab014},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, USSR Academy of Sciences, Gatchina},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={6390499},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Recombination of episomic and integrative plasmids under conditions of cotransformation of Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Kozhina, T.; Chepurnaya, O.; and Peshekhonov, V.\n\n\n \n\n\n\n Genetika, 20(6): 915-923. 1984.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Recombination$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Kozhina1984915,\r\nauthor={Kozhina, T.N. and Chepurnaya, O.V. and Peshekhonov, V.T.},\r\ntitle={Recombination of episomic and integrative plasmids under conditions of cotransformation of Saccharomyces cerevisiae},\r\njournal={Genetika},\r\nyear={1984},\r\nvolume={20},\r\nnumber={6},\r\npages={915-923},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021141457&partnerID=40&md5=532213954987f05149146755fb15c24c},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n

\n\n\n\n\n\n

\n

\n \n 1983\n \n \n (4)\n \n \n

\n

\n \n \n

\n \n\n \n \n \n \n \n \n Modeling the effects of radiation damage to DNA and the genetic risk of radionuclide decay. Dehydrogenation of pyrimidine nucleotides during decay of incorporated 3H [Modelirovanie éffektov radiatsionnykh povrezhdeniǐ DNK i geneticheskaia opasnost' raspada radionuklidov. Degidrirovanie pirimidinovykh nukleotidov pri raspade inkorpororovannogo 3H.].\n \n \n \n \n\n\n \n Korolev, V.; and Ivanov, E.\n\n\n \n\n\n\n Radiobiologiya, 23(4): 458-461. 1983.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Modeling$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1983458,\r\nauthor={Korolev, V.G. and Ivanov, E.L.},\r\ntitle={Modeling the effects of radiation damage to DNA and the genetic risk of radionuclide decay. Dehydrogenation of pyrimidine nucleotides during decay of incorporated 3H [Modelirovanie éffektov radiatsionnykh povrezhdeniǐ DNK i geneticheskaia opasnost' raspada radionuklidov. Degidrirovanie pirimidinovykh nukleotidov pri raspade inkorpororovannogo 3H.]},\r\njournal={Radiobiologiya},\r\nyear={1983},\r\nvolume={23},\r\nnumber={4},\r\npages={458-461},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0020794803&partnerID=40&md5=710eacee616df30caf28e1ab24e0b284},\r\nabstract={Dehydrogenation of DNA pyrimidine nucleotides in thymine positions 5 and 6 and cytosine position 5 is not a drastic lethal damage. Moreover, dehydrogenation of DNA in thymine positions 5 and 6 is not an effective mutagenic lesion. DNA dehydrogenation in cytosine position 5 has proved to be a pronounced mutagenic damage. As to induction of point mutations, 3H is not more harmful than external gamma-radiation given in equivalent doses.},\r\ncorrespondence_address1={Korolev, V.G.},\r\nissn={00338192},\r\npubmed_id={6351160},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiobiologiia},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Molecular nature of direct gene mutations induced by gamma and ultraviolet irradiation in Saccharomyces cerevisiae yeasts [Molekuliarnaia priroda priamykh gennykh mutatsii, indutsirovannykh gamma i ul'trafioletovym izlucheniem u drozhzheǐ Saccharomyces cerevisiae.].\n \n \n \n \n\n\n \n Ivanov, E.; Koval'tsova, S.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 19(7): 1063-1069. 1983.\n cited By 7\n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Ivanov19831063,\r\nauthor={Ivanov, E.L. and Koval'tsova, S.V. and Korolev, V.G.},\r\ntitle={Molecular nature of direct gene mutations induced by gamma and ultraviolet irradiation in Saccharomyces cerevisiae yeasts [Molekuliarnaia priroda priamykh gennykh mutatsii, indutsirovannykh gamma i ul'trafioletovym izlucheniem u drozhzheǐ Saccharomyces cerevisiae.]},\r\njournal={Genetika},\r\nyear={1983},\r\nvolume={19},\r\nnumber={7},\r\npages={1063-1069},\r\nnote={cited By 7},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0020793874&partnerID=40&md5=36ee83e009b143d7b195940bf1481809},\r\nabstract={The spectrum of gamma- and UV-induced mutations for ADE2 locus of the yeast Saccharomyces cerevisiae was determined as follows (respectively): 27 and 41% GC leads to AT transitions, 8 and 11% AT leads to GC transitions, 59 and 40% transversions, 6 and 8% frameshifts. Our results indicate a specificity of UV-light for GC leads to AT transitions. Experimental data are discussed in a view of molecular mechanisms of radiation mutagenesis.},\r\ncorrespondence_address1={Ivanov, E.L.},\r\nissn={00166758},\r\npubmed_id={6352407},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

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\n\n\n

\n \n\n \n \n \n \n \n \n Molecular nature of the mutations in gene ADE2 in Saccharomyces cerevisiae yeasts. III. Determination of the correlation of the GC AT pairs in genes ADE1 and ADE2 [Izuchenie molekuliarnoǐ prirody mutatsiǐ v gene ADE2 u drozhzheǐ Saccharomyces cerevisiae. Soobshchenie III. Opredelenie sootnosheniia par GTs i AT v genakh ADE1 i ADE2.].\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Genetika, 19(6): 921-926. 1983.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1983921,\r\nauthor={Korolev, V.G.},\r\ntitle={Molecular nature of the mutations in gene ADE2 in Saccharomyces cerevisiae yeasts. III. Determination of the correlation of the GC AT pairs in genes ADE1 and ADE2 [Izuchenie molekuliarnoǐ prirody mutatsiǐ v gene ADE2 u drozhzheǐ Saccharomyces cerevisiae. Soobshchenie III. Opredelenie sootnosheniia par GTs i AT v genakh ADE1 i ADE2.]},\r\njournal={Genetika},\r\nyear={1983},\r\nvolume={19},\r\nnumber={6},\r\npages={921-926},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-18244426544&partnerID=40&md5=f4234a71c40d0dd6570168bbe5258f7b},\r\nabstract={Lethal and mutagenic effects and the nature of mutations induced by decay of 32P incorporated into yeast cell DNA as 32P-deoxyguanosine monophosphate (32PdGMP) and 32P-thymidine monophosphate (32P-TMP), were studied. The lethal efficiency per 32P decay is independent of a labelled nucleotide incorporated into DNA. However, the mutagenic efficiency in ADE1, ADE2 genes per 32P decay is approximately 3 times greater for 32PdGMP than for 32P-TMP. This suggests that ADE1, ADE2 genes contain about 3 times more GC base pairs than AT pairs. Variations in a relative frequencies of GC leads to AT and AT leads to GC transitions were obtained depending upon a nucleotide labelled.},\r\ncorrespondence_address1={Korolev, V.G.},\r\nissn={00166758},\r\npubmed_id={6350110},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Introduction of the transposon Tn9 into the shuttle (Escherichia coli - Saccharomyces cerevisiae) plasmids and expression of the prokaryotic cam(r) gene controlling yeast cell resistance to chloramphenicol.\n \n \n \n \n\n\n \n Fedorova, I.; Kozhina, T.; and Peshekhonov, V.\n\n\n \n\n\n\n Genetika, 19(4): 541-547. 1983.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Introduction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Fedorova1983541,\r\nauthor={Fedorova, I.V. and Kozhina, T.N. and Peshekhonov, V.T.},\r\ntitle={Introduction of the transposon Tn9 into the shuttle (Escherichia coli - Saccharomyces cerevisiae) plasmids and expression of the prokaryotic cam(r) gene controlling yeast cell resistance to chloramphenicol},\r\njournal={Genetika},\r\nyear={1983},\r\nvolume={19},\r\nnumber={4},\r\npages={541-547},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0020581797&partnerID=40&md5=b19bc039010dee2c0b17be34156ee59b},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Gatchina},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={6305766},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n

\n\n\n\n\n\n

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\n \n 1981\n \n \n (4)\n \n \n

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\n \n\n \n \n \n \n \n \n Repair and mutagenesis in Escherichia coli cells upon induction in DNA of monoadducts and cross-links by light-activated 8-methoxypsoralen. Dependence of these processes on the uvrA and polA genes.\n \n \n \n \n\n\n \n Peshekhonov, V.; and Tarasov, V.\n\n\n \n\n\n\n Genetika, 17(11): 1945-1951. 1981.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Repair$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Peshekhonov19811945,\r\nauthor={Peshekhonov, V.T. and Tarasov, V.A.},\r\ntitle={Repair and mutagenesis in Escherichia coli cells upon induction in DNA of monoadducts and cross-links by light-activated 8-methoxypsoralen. Dependence of these processes on the uvrA and polA genes},\r\njournal={Genetika},\r\nyear={1981},\r\nvolume={17},\r\nnumber={11},\r\npages={1945-1951},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0019765726&partnerID=40&md5=5832d3f2aa14e3cd08e41938b25c5c9e},\r\naffiliation={Inst. Gen. Genet., Acad. Sci. USSR, Moscow 117809},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={7033042},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic effects of the breakdown of tritium incorporated into Saccharomyces cerevisiae yeast cells. IV. The lethal and mutagenic effects and the nature of the mutations induced by tritium breakdown in the 5th position of cytosine [Geneticheskie éffekty raspada tritiia, inkorporirovannogo v kletki drozhzheǐ Saccharomyces cerevisiae. Soobshchenie IV. Letal'nyǐ i mutagennyǐ éffekty i priroda mutatsiǐ, indutsirovannykh raspadom tritiia v piatom polozhenii tsitozina.].\n \n \n \n \n\n\n \n Ivanov, E.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 17(6): 1000-1008. 1981.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Ivanov19811000,\r\nauthor={Ivanov, E.L. and Korolev, V.G.},\r\ntitle={Genetic effects of the breakdown of tritium incorporated into Saccharomyces cerevisiae yeast cells. IV. The lethal and mutagenic effects and the nature of the mutations induced by tritium breakdown in the 5th position of cytosine [Geneticheskie éffekty raspada tritiia, inkorporirovannogo v kletki drozhzheǐ Saccharomyces cerevisiae. Soobshchenie IV. Letal'nyǐ i mutagennyǐ éffekty i priroda mutatsiǐ, indutsirovannykh raspadom tritiia v piatom polozhenii tsitozina.]},\r\njournal={Genetika},\r\nyear={1981},\r\nvolume={17},\r\nnumber={6},\r\npages={1000-1008},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-17744409895&partnerID=40&md5=9a345efa493704b2cf31df2be12bf4c3},\r\nabstract={We have studied in lethal and mutagenic effects and the nature of mutations induced by 3H decays in the 5-th position of cytosine (5-3H-C). The lethal efficiency was determined as alpha 1 = (10.3 +/- 6.7) x 10(-3) decay-1 or alpha 1 = (12.9 +/- 9.4) x 10(-5) rad-1 and the mutagen efficiency for ade1, ade2 genes -- as alpha m = (4.3 +/- 2.3) x 10(-7) decay-1 or alpha m = (5.4 +/- 2.9) x 10(-9) rad-1. For ade2 gene the spectrum of mutations induced by 5-3H-C was as follows: 1% of frameshifts and 99% of base pair substitutions -- 9% of transversions, 3% of AT leads to GC transitions and 87% of GC leads to AT transitions. Our results establish the 5-3H-C as one of the most effective and specific mutagens reported so far for yeast. According to the scheme of Krasin with coworkers, the final product of 3H decay in the 5-th position of cytosine is uracil. Our calculations show that more than 90% of uracil residues are removed from the yeast genome by cell repair systems.},\r\ncorrespondence_address1={Ivanov, E.L.},\r\nissn={00166758},\r\npubmed_id={7019004},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic effects of tritium decay incorporated into cells of yeast Saccharomyces cerevisiae. III. Lethal and mutagenic effects and the nature of mutations induced by 3H decay in the 5th position of thymine.\n \n \n \n \n\n\n \n Ivanov, E.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 17(2): 274-281. 1981.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Ivanov1981274,\r\nauthor={Ivanov, E.L. and Korolev, V.G.},\r\ntitle={Genetic effects of tritium decay incorporated into cells of yeast Saccharomyces cerevisiae. III. Lethal and mutagenic effects and the nature of mutations induced by 3H decay in the 5th position of thymine},\r\njournal={Genetika},\r\nyear={1981},\r\nvolume={17},\r\nnumber={2},\r\npages={274-281},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0019475166&partnerID=40&md5=42e25be8cfd1a34e8d4f1d0dbd607a48},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Gatchina},\r\nabstract={The lethal and mutagenic effects and the nature of mutations induced by 3H decays in the 5-th position of thymine (5-3H-T) were studied. The lethal efficiency was determined as α(i)=(8.8±3.0)x10-3 decay-1 or α(i)=(11.0±3.8)x10-5 rad-1 and the mutagen efficiency for ade1, ade2 genes - as α(M)=(3.7±1.3)x10-8 decay-1 or α(M)=(4.6±1.6)x10-10 rad-1. For ade2 locus the spectrum of mutations induced by 5-3H-T was as follows: 11% of frameshifts and 89% of base pair substitutions - 46% of transversions, 29% of GC→AT transitions and 14% of AT→GC transitions. As the lethal and mutagenic effects and the nature of induced mutations for 5-3H-T were similar to those of 3H-alanine, we can conclude that the local transmutation effect does not affect the genetic consequences of 3H decays in the 5-th position of thymine. The scheme was put forward establishing the 5-hydroxymethyluracil (5-HMU) as the final product of methyl-3H-thymine decay. The data available suggest that 5-HMU is either effectively removed from DNA or makes for retaining the coding ability of thymine.},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Genetic effects of tritium decay incorporated into cells of yeast Saccharomyces cerevisiae. II. Mutagenic effect of 3H-alanine and the nature of mutations induced.\n \n \n \n \n\n\n \n Ivanov, E.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 17(2): 268-273. 1981.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Ivanov1981268,\r\nauthor={Ivanov, E.L. and Korolev, V.G.},\r\ntitle={Genetic effects of tritium decay incorporated into cells of yeast Saccharomyces cerevisiae. II. Mutagenic effect of 3H-alanine and the nature of mutations induced},\r\njournal={Genetika},\r\nyear={1981},\r\nvolume={17},\r\nnumber={2},\r\npages={268-273},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0019461238&partnerID=40&md5=254ef337470755166f01a873034b3b13},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Gatchina},\r\nabstract={The mutagenic effect and the nature of mutations induced by tritium decay in the form of 3H-alanine were studied. The efficiency of mutation production in ade1 and ade2 genes is αm = (8.5 ± 3.6) x 10-10 decay(-1) or αm = (7.7 ± 3.3) x 10-10 rad(-1). The relative mutagenic efficiency (RME) of tritium β-particles was established as 0.3-0.4 compared with (32)P β-particles. The spectrum of induced mutations for the ade2 locus was represented by 8% frameshifts and 92% base pair substitutions (GC→AT transitions - 20%, AT→GC transitions - 12% and transversions - 60%). Among missense-mutations 58% were transversions and 42% transitions: 22% GC→AT and 20% AT→GC.},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n\n\n

\n

\n \n 1980\n \n \n (2)\n \n \n

\n

\n \n \n

\n \n\n \n \n \n \n \n \n Nuclear nature of mutations in ade2 gene of Saccharomyces cerevisiae. II. Analysis of non-complementating and polar-complementating mutations.\n \n \n \n \n\n\n \n Gracheva, L.; Korolev, V.; and Ivanov, E.\n\n\n \n\n\n\n Genetika, 16(3): 418-425. 1980.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Nuclear$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Gracheva1980418,\r\nauthor={Gracheva, L.M. and Korolev, V.G. and Ivanov, E.L.},\r\ntitle={Nuclear nature of mutations in ade2 gene of Saccharomyces cerevisiae. II. Analysis of non-complementating and polar-complementating mutations},\r\njournal={Genetika},\r\nyear={1980},\r\nvolume={16},\r\nnumber={3},\r\npages={418-425},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0018901804&partnerID=40&md5=0b3e1654cb7f140c51156fb192e8e906},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Gatchina},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Nuclear nature of mutations in ade2 gene of Saccharomyces cerevisiae. I. General scheme and analysis of non-polar complementing mutations.\n \n \n \n \n\n\n \n Korolev, V.; Ivanov, E.; and Gracheva, L.\n\n\n \n\n\n\n Genetika, 16(2): 230-238. 1980.\n cited By 6\n\n\n\n
\n\n\n\n \n \n $\"Nuclear$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1980230,\r\nauthor={Korolev, V.G. and Ivanov, E.L. and Gracheva, L.M.},\r\ntitle={Nuclear nature of mutations in ade2 gene of Saccharomyces cerevisiae. I. General scheme and analysis of non-polar complementing mutations},\r\njournal={Genetika},\r\nyear={1980},\r\nvolume={16},\r\nnumber={2},\r\npages={230-238},\r\nnote={cited By 6},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0018828926&partnerID=40&md5=325b88ca82b5d0690a59aec5be77927e},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Scis USSR, Gatchina, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n

\n\n\n\n\n\n

\n

\n \n 1979\n \n \n (1)\n \n \n

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\n \n \n

\n \n\n \n \n \n \n \n \n Genetic effects of 35S decay in cells of the yeast Saccharomyces cerevisiae. V. Comparative studies of the lethal and mutagenic effects of decays of 35S and 32P incorporated into cells of radiation sensitive mutant XRS2.\n \n \n \n \n\n\n \n Korolev, V.; and Ivanov, E.\n\n\n \n\n\n\n Genetika, 15(6): 1024-1032. 1979.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev19791024,\r\nauthor={Korolev, V.G. and Ivanov, E.L.},\r\ntitle={Genetic effects of 35S decay in cells of the yeast Saccharomyces cerevisiae. V. Comparative studies of the lethal and mutagenic effects of decays of 35S and 32P incorporated into cells of radiation sensitive mutant XRS2},\r\njournal={Genetika},\r\nyear={1979},\r\nvolume={15},\r\nnumber={6},\r\npages={1024-1032},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0018483772&partnerID=40&md5=a7ba78e14a6fed28d8909ae616d524b5},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nabstract={The lethal effect of 35S and 32P decays on cells of yeast radiation-sensitive mutant xrs2 was studied. The mutant is 7 times more sensitive than the wild type to transmutation of both isotopes. The survival curve for xrs2 was exponential. In spite of the lethal effect, mutant cells are not more mutable than the wild type under decay of both isotopes (the number of mutations in ade1 and ade2 genes was counted). xrs2 and wild type strains differ in kinds of mutations induced by the decay of incorporated 35S in ade2 locus. Namely, there are 82% of base substitutions and 18% of other type mutations induced in xrs2 strain, despite 97% and 3%, respectively, for the wild type strain. Also it was shown that complete and mosaic mutants, induced by the 35S decay in xrs2 strain, differ in a pattern of interallelic complementation.},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={381101},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

\n

\n \n 1978\n \n \n (2)\n \n \n

\n

\n \n \n

\n \n\n \n \n \n \n \n \n Genetic effects of tritium decay incorporated in cells of yeast Saccharomyces cerevisiae. I. Lethal effect of 3H alanine on cells of different ploidy and radiosensitivity.\n \n \n \n \n\n\n \n Korolev, V.; and Gracheva, L.\n\n\n \n\n\n\n Genetika, 14(2): 328-333. 1978.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1978328,\r\nauthor={Korolev, V.G. and Gracheva, L.M.},\r\ntitle={Genetic effects of tritium decay incorporated in cells of yeast Saccharomyces cerevisiae. I. Lethal effect of 3H alanine on cells of different ploidy and radiosensitivity},\r\njournal={Genetika},\r\nyear={1978},\r\nvolume={14},\r\nnumber={2},\r\npages={328-333},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0017797269&partnerID=40&md5=1e03d38013612cf08a2101fcce662d71},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={357247},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

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\n \n\n \n \n \n \n \n \n Mutagenic effect of the decay of 32P incorporated in mRNA.\n \n \n \n \n\n\n \n Zakharov, I.; Korolev, V.; and Gracheva, L.\n\n\n \n\n\n\n Genetika, 14(10): 1838-1841. 1978.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Mutagenic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Zakharov19781838,\r\nauthor={Zakharov, I.A. and Korolev, V.G. and Gracheva, L.M.},\r\ntitle={Mutagenic effect of the decay of 32P incorporated in mRNA},\r\njournal={Genetika},\r\nyear={1978},\r\nvolume={14},\r\nnumber={10},\r\npages={1838-1841},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0018196086&partnerID=40&md5=8d003e4211f013293cc43dfede80735a},\r\naffiliation={B. P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={363507},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

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\n \n 1977\n \n \n (1)\n \n \n

\n

\n \n \n

\n \n\n \n \n \n \n \n \n Genealogical characteristics and genetic parameters of cattle herd of Elansky tribal plant.\n \n \n \n \n\n\n \n Korolev, V.\n\n\n \n\n\n\n Genetika, 13(10): 1754-1760. 1977.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genealogical$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev19771754,\r\nauthor={Korolev, V.G.},\r\ntitle={Genealogical characteristics and genetic parameters of cattle herd of Elansky tribal plant},\r\njournal={Genetika},\r\nyear={1977},\r\nvolume={13},\r\nnumber={10},\r\npages={1754-1760},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0017707613&partnerID=40&md5=05fa4c5984f89391d36b6103239b2118},\r\naffiliation={V.V. Dokuchaev Res. Inst. Agricult., Cent. Chernozem Zone, Voronezh, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1976\n \n \n (3)\n \n \n

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\n \n\n \n \n \n \n \n \n Genetic effects of 35S decay in cells of yeast Saccharomyces cerevisiae. IV. Dependence of the lethal effect of 35S decay on the inclusion in different sulphur containing molecules of cell (Russian).\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 12(1): 111-115. 1976.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Gracheva1976111,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={Genetic effects of 35S decay in cells of yeast Saccharomyces cerevisiae. IV. Dependence of the lethal effect of 35S decay on the inclusion in different sulphur containing molecules of cell (Russian)},\r\njournal={Genetika},\r\nyear={1976},\r\nvolume={12},\r\nnumber={1},\r\npages={111-115},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0017288576&partnerID=40&md5=d8a5a580ed5196987a91314a74558217},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Genetic effects of 35S decay in cells of yeast Saccharomyces cerevisiae. III. Recombinogenic effect (Russian).\n \n \n \n \n\n\n \n Korolev, V.; and Gracheva, L.\n\n\n \n\n\n\n Genetika, 12(1): 160-162. 1976.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1976160,\r\nauthor={Korolev, V.G. and Gracheva, L.M.},\r\ntitle={Genetic effects of 35S decay in cells of yeast Saccharomyces cerevisiae. III. Recombinogenic effect (Russian)},\r\njournal={Genetika},\r\nyear={1976},\r\nvolume={12},\r\nnumber={1},\r\npages={160-162},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0017253231&partnerID=40&md5=250042d20642e30b7a0e353aaf8d7420},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n

\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Lethal effect of 32P decay incorporated in cells and zygotes of Saccharomyces cerevisiae of different ploidy and with different number of labelled genomes (Russian).\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 12(9): 95-103. 1976.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Lethal$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva197695,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={Lethal effect of 32P decay incorporated in cells and zygotes of Saccharomyces cerevisiae of different ploidy and with different number of labelled genomes (Russian)},\r\njournal={Genetika},\r\nyear={1976},\r\nvolume={12},\r\nnumber={9},\r\npages={95-103},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0017105505&partnerID=40&md5=8bcf500923d176b3b91244c157326682},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nabstract={The lethal effects of 32P decay in cells and zygotes of different ploidy and with different number of labelled genomes was studied. All the strains studied were divided into three groups for the value of lethal efficiency. Strains of the first group had values of the lethal efficiency similar to those for haploid cells. In this group enter haploid cells, diploid zygotes with one and two labelled genomes, triploid zygotes with one labelled genome and a diploid, homozygous for the mutation to X ray sensitivity. Strains of the second group have the lethal efficiency approximately 5 fold as low as strains of the first group. In the second group enter di, tri and tetraploid cells, triploid zygotes with two labelled genomes and budded cells. A possible role of mitotic recombination in the resistance to 32P decay of strains of the second group is discussed.},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

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\n \n 1974\n \n \n (5)\n \n \n

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\n \n \n

\n \n\n \n \n \n \n \n \n Induction and inactivation of cytoductants in Saccharomyces cerevisiae by P 32 decay.\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n SOV.GENET., 8(10): 1303-1306. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Induction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva19741303,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={Induction and inactivation of cytoductants in Saccharomyces cerevisiae by P 32 decay},\r\njournal={SOV.GENET.},\r\nyear={1974},\r\nvolume={8},\r\nnumber={10},\r\npages={1303-1306},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016317711&partnerID=40&md5=7b351967f4366a76d8f3da0120ad20b1},\r\naffiliation={A.F. Ioffe Physicotechn. Inst., Acad. Sci. USSR, Gatchina, Russia},\r\nabstract={Cytoduction is effectively induced during conjugation of haploid cells previously damaged by decay of incorporated P 32 . The greatest cytoduction effect is observed after damage to the nucleus of the cell acting as donor of the cytoplasm. Induction of cytoductants takes place during conjugation and the accumulation of damage during preservation of the zygotes does not lead to any increase in the percentage of cytoductants.},\r\ncoden={SOGEB},\r\npubmed_id={4612739},\r\nlanguage={English},\r\nabbrev_source_title={SOV.GENET.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n The role of β radiation, accompanying the decay of phosphorus 32 incorporated into the cells of diploid yeasts, in the induction of recombination.\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n SOV.GENET., 8(9): 1139-1145. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Gracheva19741139,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={The role of β radiation, accompanying the decay of phosphorus 32 incorporated into the cells of diploid yeasts, in the induction of recombination},\r\njournal={SOV.GENET.},\r\nyear={1974},\r\nvolume={8},\r\nnumber={9},\r\npages={1139-1145},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016300143&partnerID=40&md5=4d84dd08855e62fc79f734f1bef71fef},\r\naffiliation={A.F. Ioffe Phys. Techn. Inst., Acad. Scis USSR, Leningrad, Russia},\r\nabstract={β radiation effectively induces mitotic recombination. It is shown that the effect of external β radiation in the induction of recombination is = 25% of the summary effect of transmutation and β radiation. Calculations of the dose of β radiation on the nucleus of the yeast cell in the case of external and internal β radiation are presented.},\r\ncoden={SOGEB},\r\npubmed_id={4610784},\r\nlanguage={English},\r\nabbrev_source_title={SOV.GENET.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic effects of 35S decay in cells of the yeast Saccharomyces cerevisiae. I. Lethal effect of decay of 35S incorporated in cells of different ploidy and radiosensitivity (Russian).\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n Genetika, 10(6): 70-77. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva197470,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={Genetic effects of 35S decay in cells of the yeast Saccharomyces cerevisiae. I. Lethal effect of decay of 35S incorporated in cells of different ploidy and radiosensitivity (Russian)},\r\njournal={Genetika},\r\nyear={1974},\r\nvolume={10},\r\nnumber={6},\r\npages={70-77},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016208365&partnerID=40&md5=6c6801c2fd8ce980fc6bc552988a48fa},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nabstract={The lethal effect of 35S decay on cells of yeast Saccharomyces cerevisiae of different ploidy was studied. It is shown that the efficiency of incorporation of 35S is practically equal to the efficiency of incorporation of 32P and it is 10 times higher than external β radiation. Triploid and tetraploid cells have the same radioresistance but the diploid cells have a slightly higher sensitivity. They are more radioresistant than the haploid. The diploid xrs2 is less radioresistant than the wild type diploid but it is more radioresistant than the haploid. The existence of structures sensitive to 35S decay in cells of eukaryotes is discussed.},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic effects of 35S decay in cells of the yeast Saccharomyces cerevisiae. II. Mutagenic effect and the nature of the induced mutations (Russian).\n \n \n \n \n\n\n \n Korolev, V.; Gracheva, L.; and Bolotnikova, E.\n\n\n \n\n\n\n Genetika, 10(7): 91-96. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev197491,\r\nauthor={Korolev, V.G. and Gracheva, L.M. and Bolotnikova, E.V.},\r\ntitle={Genetic effects of 35S decay in cells of the yeast Saccharomyces cerevisiae. II. Mutagenic effect and the nature of the induced mutations (Russian)},\r\njournal={Genetika},\r\nyear={1974},\r\nvolume={10},\r\nnumber={7},\r\npages={91-96},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016170185&partnerID=40&md5=2909b6de12a0350a2e828e072961cab5},\r\naffiliation={B. P. Konstantinov Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad, Russian Federation},\r\nabstract={The induction of mutations in haploid cells of the yeast Saccharomyces cerevisiae by the decay of incorporated radioactive sulfur was studied. The mutagenic effect of 35S was compared with that of incorporated 32P and external β radiation. Incorporated 35S was about as effective as 32P and 15 times more effective than external β radiation. Complementation tests were made on 139 ade mutants induced by the decay of 35S. The ratio of mutations at the adenine requirement loci, ade1 and ade2, was 1 : 2.5. As regards the nature of the mutations, 35S mutants (93%) carried mutations of the base exchange type.},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Comparative studies of the mutagenic effects of external β irradiation and of incorporated radiophosphorus (32P) on haploid cells of yeast and on the nature of the mutations induced by these agents (Russian).\n \n \n \n \n\n\n \n Korolev, V.; Grachiova, L.; and Bolotnikova, E.\n\n\n \n\n\n\n Genetika, 10(3): 111-119. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Comparative$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev1974111,\r\nauthor={Korolev, V.G. and Grachiova, L.M. and Bolotnikova, E.V.},\r\ntitle={Comparative studies of the mutagenic effects of external β irradiation and of incorporated radiophosphorus (32P) on haploid cells of yeast and on the nature of the mutations induced by these agents (Russian)},\r\njournal={Genetika},\r\nyear={1974},\r\nvolume={10},\r\nnumber={3},\r\npages={111-119},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015950223&partnerID=40&md5=fb39eb86e7846394d2c1370ec1cf1fdc},\r\naffiliation={B.P. Konstantinov Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad},\r\nissn={00166758},\r\ncoden={GNKAA},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1973\n \n \n (3)\n \n \n

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\n \n\n \n \n \n \n \n \n Induction of recombination in yeasts in the presence of decay of incorporated phosphorus 32.\n \n \n \n \n\n\n \n Korolev, V.; and Gracheva, L.\n\n\n \n\n\n\n SOV.GENET., 7(2): 245-249. 1973.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Induction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@ARTICLE{Korolev1973245,\r\nauthor={Korolev, V.G. and Gracheva, L.M.},\r\ntitle={Induction of recombination in yeasts in the presence of decay of incorporated phosphorus 32},\r\njournal={SOV.GENET.},\r\nyear={1973},\r\nvolume={7},\r\nnumber={2},\r\npages={245-249},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015704308&partnerID=40&md5=5fb80c283bdb1b4e33d644d67305c611},\r\naffiliation={A.F. Ioffe Physicotechn. Inst., Leningrad, Russia},\r\ncoden={SOGEB},\r\npubmed_id={4804066},\r\nlanguage={English},\r\nabbrev_source_title={SOV.GENET.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic nature of mutations in yeasts, induced by different radiations and arising against a background of different genotypes [Geneticheskaia priroda mutatsiǐ u drozhzheǐ, indutsirovannykh raznymi izlucheniiami i voznikaiushchikh na fone razlichnogo genotipa.].\n \n \n \n \n\n\n \n Zakharov, I.; Gracheva, L.; Koval'tsova, S.; Kozhina, T.; and Korolev, V.\n\n\n \n\n\n\n Doklady Akademii nauk SSSR, 212(6): 1445-1447. 1973.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Zakharov19731445,\r\nauthor={Zakharov, I.A. and Gracheva, L.M. and Koval'tsova, S.V. and Kozhina, T.N. and Korolev, V.G.},\r\ntitle={Genetic nature of mutations in yeasts, induced by different radiations and arising against a background of different genotypes [Geneticheskaia priroda mutatsiǐ u drozhzheǐ, indutsirovannykh raznymi izlucheniiami i voznikaiushchikh na fone razlichnogo genotipa.]},\r\njournal={Doklady Akademii nauk SSSR},\r\nyear={1973},\r\nvolume={212},\r\nnumber={6},\r\npages={1445-1447},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015932353&partnerID=40&md5=035f14dad534001b46ee8390cf1f313d},\r\ncorrespondence_address1={Zakharov, I.A.},\r\nissn={00023264},\r\npubmed_id={4754232},\r\nlanguage={Russian},\r\nabbrev_source_title={Dokl Akad Nauk SSSR},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Effects of the decay of radiophosphorus on haploid and diploid cells of the yeast Saccharomyces cerevisiae of different genotypes.\n \n \n \n \n\n\n \n Gracheva, L.; Zheleznyakova, N.; and Korolev, V.\n\n\n \n\n\n\n SOV.GENET., 6(12): 1629-1632. 1973.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Effects$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva19731629,\r\nauthor={Gracheva, L.M. and Zheleznyakova, N.Y. and Korolev, V.G.},\r\ntitle={Effects of the decay of radiophosphorus on haploid and diploid cells of the yeast Saccharomyces cerevisiae of different genotypes},\r\njournal={SOV.GENET.},\r\nyear={1973},\r\nvolume={6},\r\nnumber={12},\r\npages={1629-1632},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015887238&partnerID=40&md5=442f142f3c7b238e17af9467e5671d30},\r\naffiliation={A.F. Ioffe Physicotechn. Inst., Acad. Sci. USSR, Leningrad},\r\nabstract={Experiments were conducted on the inactivation by the decay of incorporated radiophosphorus of haploid and diploid yeast strains with different sensitivities to UV and x rays. The coefficient α for the haploid strain proved equal to 0.016 ± 0.001, for the initial strain of diploid yeasts PG-60 0.0014 ± 0.0001, for the UV sensitive strain PG 61 0.0019 ± 0.0002, and for the x ray sensitive strain PG-74 0.0051 ± 0.0009. The dose vs effect dependence for 15-VP-4 and PG-74 was exponential, and that for PG-60 and PG-61 sigmoid. The dependence of the rate of inactivation on the specific activity was a direct proportionality.},\r\ncoden={SOGEB},\r\nlanguage={English},\r\nabbrev_source_title={SOV.GENET.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1972\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n Induction of recombination by the decay of phosphorus 32 incorporated into one or both genomes of the zygote of the yeast Saccharomyces cerevisiae.\n \n \n \n \n\n\n \n Korolev, V.; and Gracheva, L.\n\n\n \n\n\n\n SOV.GENET., 8(8): 1031-1037. 1972.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Induction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Korolev19721031,\r\nauthor={Korolev, V.G. and Gracheva, L.M.},\r\ntitle={Induction of recombination by the decay of phosphorus 32 incorporated into one or both genomes of the zygote of the yeast Saccharomyces cerevisiae},\r\njournal={SOV.GENET.},\r\nyear={1972},\r\nvolume={8},\r\nnumber={8},\r\npages={1031-1037},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015438453&partnerID=40&md5=36a34574417837dca7db0ff39c88276b},\r\naffiliation={A.F. Ioffe Physicotechn. Inst., Acad. Sci. USSR, Leningrad, Russian Federation},\r\ncoden={SOGEB},\r\nlanguage={English},\r\nabbrev_source_title={SOV.GENET.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1971\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n Biological effects of the decay of radiophosphorus incorporated into cells of microorganism [Bailogicheskie posledstviia raspada radiofosfora inkorporirovannogo v kletki mikroorganizmov.].\n \n \n \n \n\n\n \n Gracheva, L.; and Korolev, V.\n\n\n \n\n\n\n Uspekhi sovremennoi biologii, 72(1): 143-158. 1971.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Biological$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@ARTICLE{Gracheva1971143,\r\nauthor={Gracheva, L.M. and Korolev, V.G.},\r\ntitle={Biological effects of the decay of radiophosphorus incorporated into cells of microorganism [Bailogicheskie posledstviia raspada radiofosfora inkorporirovannogo v kletki mikroorganizmov.]},\r\njournal={Uspekhi sovremennoi biologii},\r\nyear={1971},\r\nvolume={72},\r\nnumber={1},\r\npages={143-158},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015084473&partnerID=40&md5=129616c32b3ff94b3d87b635749b9316},\r\ncorrespondence_address1={Gracheva, L.M.},\r\nissn={00421324},\r\npubmed_id={4944704},\r\nlanguage={Russian},\r\nabbrev_source_title={Usp Sovrem Biol},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n

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\n \n undefined\n \n \n (10)\n \n \n

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