@article{dohmann_arabidopsis_2008,
	title = {The {Arabidopsis} {COP9} signalosome is essential for {G2} phase progression and genomic stability},
	volume = {135},
	issn = {0950-1991},
	doi = {10/b8t2wz},
	abstract = {The COP9 signalosome (CSN) is required for the full activity of cullin-RING E3 ubiquitin ligases (CRLs) in eukaryotes. CSN exerts its function on CRLs by removing the ubiquitin-related NEDD8 conjugate from the cullin subunit of CRLs. CSN seems, thereby, to control CRL disassembly or CRL subunit stability. In Arabidopsis thaliana, loss of CSN function leads to constitutive photomorphogenic (cop) seedling development and a post-germination growth arrest. The underlying molecular cause of this growth arrest is currently unknown. Here, we show that Arabidopsis csn mutants are delayed in G2 phase progression. This cell cycle arrest correlates with the induction of the DNA damage response pathway and is suggestive of the activation of a DNA damage checkpoint. In support of this hypothesis, we detected gene conversion events in csn mutants that are indicative of DNA double-strand breaks. DNA damage is also apparent in mutants of the NEDD8 conjugation pathway and in mutants of the E3 ligase subunits CULLIN4, COP1 and DET1, which share phenotypes with csn mutants. In summary, our data suggest that Arabidopsis csn mutants undergo DNA damage, which might be the cause of the delay in G2 cell cycle progression.},
	language = {eng},
	number = {11},
	journal = {Development (Cambridge, England)},
	author = {Dohmann, Esther M. N. and Levesque, Mitchell P. and De Veylder, Lieven and Reichardt, Ilka and Jürgens, Gerd and Schmid, Markus and Schwechheimer, Claus},
	month = jun,
	year = {2008},
	pmid = {18434413},
	keywords = {ATP-Binding Cassette Transporters, Arabidopsis Proteins, COP9 Signalosome Complex, Cell Cycle, Cell Division, Cullin Proteins, Cyclin B, DNA Damage, Flow Cytometry, G2 Phase, Gene Expression Regulation, Developmental, Gene Expression Regulation, Plant, Genomic Instability, Immunoblotting, In Situ Nick-End Labeling, Intracellular Signaling Peptides and Proteins, Multiprotein Complexes, Nuclear Proteins, Oligonucleotide Array Sequence Analysis, Peptide Hydrolases, Plant Roots, Protein Kinases, Protein-Serine-Threonine Kinases, Seedlings, Ubiquitin-Protein Ligases, Ubiquitins},
	pages = {2013--2022},
}

{"_id":"BX32TkowSDt3nWRyv","bibbaseid":"dohmann-levesque-deveylder-reichardt-jrgens-schmid-schwechheimer-thearabidopsiscop9signalosomeisessentialforg2phaseprogressionandgenomicstability-2008","author_short":["Dohmann, E. M. N.","Levesque, M. P.","De Veylder, L.","Reichardt, I.","Jürgens, G.","Schmid, M.","Schwechheimer, C."],"bibdata":{"bibtype":"article","type":"article","title":"The Arabidopsis COP9 signalosome is essential for G2 phase progression and genomic stability","volume":"135","issn":"0950-1991","doi":"10/b8t2wz","abstract":"The COP9 signalosome (CSN) is required for the full activity of cullin-RING E3 ubiquitin ligases (CRLs) in eukaryotes. CSN exerts its function on CRLs by removing the ubiquitin-related NEDD8 conjugate from the cullin subunit of CRLs. CSN seems, thereby, to control CRL disassembly or CRL subunit stability. In Arabidopsis thaliana, loss of CSN function leads to constitutive photomorphogenic (cop) seedling development and a post-germination growth arrest. The underlying molecular cause of this growth arrest is currently unknown. Here, we show that Arabidopsis csn mutants are delayed in G2 phase progression. This cell cycle arrest correlates with the induction of the DNA damage response pathway and is suggestive of the activation of a DNA damage checkpoint. In support of this hypothesis, we detected gene conversion events in csn mutants that are indicative of DNA double-strand breaks. DNA damage is also apparent in mutants of the NEDD8 conjugation pathway and in mutants of the E3 ligase subunits CULLIN4, COP1 and DET1, which share phenotypes with csn mutants. In summary, our data suggest that Arabidopsis csn mutants undergo DNA damage, which might be the cause of the delay in G2 cell cycle progression.","language":"eng","number":"11","journal":"Development (Cambridge, England)","author":[{"propositions":[],"lastnames":["Dohmann"],"firstnames":["Esther","M.","N."],"suffixes":[]},{"propositions":[],"lastnames":["Levesque"],"firstnames":["Mitchell","P."],"suffixes":[]},{"propositions":[],"lastnames":["De","Veylder"],"firstnames":["Lieven"],"suffixes":[]},{"propositions":[],"lastnames":["Reichardt"],"firstnames":["Ilka"],"suffixes":[]},{"propositions":[],"lastnames":["Jürgens"],"firstnames":["Gerd"],"suffixes":[]},{"propositions":[],"lastnames":["Schmid"],"firstnames":["Markus"],"suffixes":[]},{"propositions":[],"lastnames":["Schwechheimer"],"firstnames":["Claus"],"suffixes":[]}],"month":"June","year":"2008","pmid":"18434413","keywords":"ATP-Binding Cassette Transporters, Arabidopsis Proteins, COP9 Signalosome Complex, Cell Cycle, Cell Division, Cullin Proteins, Cyclin B, DNA Damage, Flow Cytometry, G2 Phase, Gene Expression Regulation, Developmental, Gene Expression Regulation, Plant, Genomic Instability, Immunoblotting, In Situ Nick-End Labeling, Intracellular Signaling Peptides and Proteins, Multiprotein Complexes, Nuclear Proteins, Oligonucleotide Array Sequence Analysis, Peptide Hydrolases, Plant Roots, Protein Kinases, Protein-Serine-Threonine Kinases, Seedlings, Ubiquitin-Protein Ligases, Ubiquitins","pages":"2013–2022","bibtex":"@article{dohmann_arabidopsis_2008,\n\ttitle = {The {Arabidopsis} {COP9} signalosome is essential for {G2} phase progression and genomic stability},\n\tvolume = {135},\n\tissn = {0950-1991},\n\tdoi = {10/b8t2wz},\n\tabstract = {The COP9 signalosome (CSN) is required for the full activity of cullin-RING E3 ubiquitin ligases (CRLs) in eukaryotes. CSN exerts its function on CRLs by removing the ubiquitin-related NEDD8 conjugate from the cullin subunit of CRLs. CSN seems, thereby, to control CRL disassembly or CRL subunit stability. In Arabidopsis thaliana, loss of CSN function leads to constitutive photomorphogenic (cop) seedling development and a post-germination growth arrest. The underlying molecular cause of this growth arrest is currently unknown. Here, we show that Arabidopsis csn mutants are delayed in G2 phase progression. This cell cycle arrest correlates with the induction of the DNA damage response pathway and is suggestive of the activation of a DNA damage checkpoint. In support of this hypothesis, we detected gene conversion events in csn mutants that are indicative of DNA double-strand breaks. DNA damage is also apparent in mutants of the NEDD8 conjugation pathway and in mutants of the E3 ligase subunits CULLIN4, COP1 and DET1, which share phenotypes with csn mutants. In summary, our data suggest that Arabidopsis csn mutants undergo DNA damage, which might be the cause of the delay in G2 cell cycle progression.},\n\tlanguage = {eng},\n\tnumber = {11},\n\tjournal = {Development (Cambridge, England)},\n\tauthor = {Dohmann, Esther M. N. and Levesque, Mitchell P. and De Veylder, Lieven and Reichardt, Ilka and Jürgens, Gerd and Schmid, Markus and Schwechheimer, Claus},\n\tmonth = jun,\n\tyear = {2008},\n\tpmid = {18434413},\n\tkeywords = {ATP-Binding Cassette Transporters, Arabidopsis Proteins, COP9 Signalosome Complex, Cell Cycle, Cell Division, Cullin Proteins, Cyclin B, DNA Damage, Flow Cytometry, G2 Phase, Gene Expression Regulation, Developmental, Gene Expression Regulation, Plant, Genomic Instability, Immunoblotting, In Situ Nick-End Labeling, Intracellular Signaling Peptides and Proteins, Multiprotein Complexes, Nuclear Proteins, Oligonucleotide Array Sequence Analysis, Peptide Hydrolases, Plant Roots, Protein Kinases, Protein-Serine-Threonine Kinases, Seedlings, Ubiquitin-Protein Ligases, Ubiquitins},\n\tpages = {2013--2022},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n","author_short":["Dohmann, E. M. N.","Levesque, M. 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