var bibbase_data = {"data":"\"Loading..\"\n\n
\n\n \n\n \n\n \n \n\n \n\n \n \n\n \n\n \n
\n generated by\n \n \"bibbase.org\"\n\n \n
\n \n\n
\n\n \n\n\n
\n\n Excellent! Next you can\n create a new website with this list, or\n embed it in an existing web page by copying & pasting\n any of the following snippets.\n\n
\n JavaScript\n (easiest)\n
\n \n <script src=\"https://bibbase.org/show?bib=https%3A%2F%2Fapi.zotero.org%2Fusers%2F3476755%2Fcollections%2FLE66JLKI%2Fitems%3Fkey%3D9MaG4TgseJqKgAFdOazlPFUw%26format%3Dbibtex%26limit%3D100&jsonp=1&authorFirst=1&hidemenu=true&commas=true&sort=author_short&groupby=&jsonp=1\"></script>\n \n
\n\n PHP\n
\n \n <?php\n $contents = file_get_contents(\"https://bibbase.org/show?bib=https%3A%2F%2Fapi.zotero.org%2Fusers%2F3476755%2Fcollections%2FLE66JLKI%2Fitems%3Fkey%3D9MaG4TgseJqKgAFdOazlPFUw%26format%3Dbibtex%26limit%3D100&jsonp=1&authorFirst=1&hidemenu=true&commas=true&sort=author_short&groupby=\");\n print_r($contents);\n ?>\n \n
\n\n iFrame\n (not recommended)\n
\n \n <iframe src=\"https://bibbase.org/show?bib=https%3A%2F%2Fapi.zotero.org%2Fusers%2F3476755%2Fcollections%2FLE66JLKI%2Fitems%3Fkey%3D9MaG4TgseJqKgAFdOazlPFUw%26format%3Dbibtex%26limit%3D100&jsonp=1&authorFirst=1&hidemenu=true&commas=true&sort=author_short&groupby=\"></iframe>\n \n
\n\n

\n For more details see the documention.\n

\n
\n
\n\n
\n\n This is a preview! To use this list on your own web site\n or create a new web site from it,\n create a free account. The file will be added\n and you will be able to edit it in the File Manager.\n We will show you instructions once you've created your account.\n
\n\n
\n\n

To the site owner:

\n\n

Action required! Mendeley is changing its\n API. In order to keep using Mendeley with BibBase past April\n 14th, you need to:\n

    \n
  1. renew the authorization for BibBase on Mendeley, and
  2. \n
  3. update the BibBase URL\n in your page the same way you did when you initially set up\n this page.\n
  4. \n
\n

\n\n

\n \n \n Fix it now\n

\n
\n\n
\n\n\n
\n \n \n
\n \n\n \n \n Cornwall, C., Comeau, S., & Harvey, B. P\n\n\n \n \n \n \n \n Physiological and ecological tipping points caused by ocean acidification.\n \n \n \n \n\n\n \n\n\n\n September 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PhysiologicalPaper\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
\n
@misc{cornwall_physiological_2023,\n\ttitle = {Physiological and ecological tipping points caused by ocean acidification},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\turl = {https://esd.copernicus.org/preprints/esd-2023-24/},\n\tdoi = {10.5194/esd-2023-24},\n\tabstract = {Abstract. Ocean acidification is predicted to cause profound shifts in many marine ecosystems by impairing the ability of calcareous taxa to calcify and grow, and by influencing the photo-physiology of many others. In both calcifying and non-calcifying taxa, ocean acidification could further impair the ability of marine life to regulate internal pH, and thus metabolic function and/or behaviour. Identifying tipping points at which these effects will occur for different taxa due to the direct impacts of ocean acidification on organism physiology is difficult and they have not adequately been determined for most taxa, nor for ecosystems at higher levels. This is due to the presence of both resistant and sensitive species within most taxa. However, calcifying taxa such as coralline algae, corals, molluscs, and sea urchins appear to be most sensitive to ocean acidification. Conversely, non-calcareous seaweeds, seagrasses, diatoms, cephalopods, and fish tend to be more resistant, or even benefit from the direct effects of ocean acidification. While physiological tipping points of the effects of ocean acidification either do not exist or are not well defined, their direct effects on organism physiology will have flow on indirect effects. These indirect effects will cause ecologically tipping points in the future through changes in competition, herbivory and predation. Evidence for indirect effects and ecological change is mostly taken from benthic ecosystems in warm temperate–tropical locations in situ that have elevated CO2. Species abundances at these locations indicate a shift away from calcifying taxa and towards non-calcareous at high CO2 concentrations. For example, lower abundance of corals and coralline algae, and higher covers of non-calcareous macroalgae, often turfing species, at elevated CO2. However, there are some locations where only minor changes, or no detectable change occurs. Where ecological tipping points do occur, it is usually at locations with naturally elevated pCO2 concentrations of 500 μatm or more, which also corresponds to just under that concentrations where the direct physiological impacts of ocean acidification are detectable on the most sensitive taxa in laboratory research (coralline algae and corals). Collectively, the available data support the concern that ocean acidification will most likely cause ecological change in the near future in most benthic marine ecosystems, with tipping points in some ecosystems at as low as 500 μatm pCO2. However, much more further research is required to more adequately quantify and model the extent of these impacts in order to accurately project future marine ecosystem tipping points under ocean acidification.},\n\turldate = {2024-04-04},\n\tauthor = {Cornwall, Christopher and Comeau, Steeve and Harvey, Ben P},\n\tmonth = sep,\n\tyear = {2023},\n}\n\n
\n
\n\n\n
\n Abstract. Ocean acidification is predicted to cause profound shifts in many marine ecosystems by impairing the ability of calcareous taxa to calcify and grow, and by influencing the photo-physiology of many others. In both calcifying and non-calcifying taxa, ocean acidification could further impair the ability of marine life to regulate internal pH, and thus metabolic function and/or behaviour. Identifying tipping points at which these effects will occur for different taxa due to the direct impacts of ocean acidification on organism physiology is difficult and they have not adequately been determined for most taxa, nor for ecosystems at higher levels. This is due to the presence of both resistant and sensitive species within most taxa. However, calcifying taxa such as coralline algae, corals, molluscs, and sea urchins appear to be most sensitive to ocean acidification. Conversely, non-calcareous seaweeds, seagrasses, diatoms, cephalopods, and fish tend to be more resistant, or even benefit from the direct effects of ocean acidification. While physiological tipping points of the effects of ocean acidification either do not exist or are not well defined, their direct effects on organism physiology will have flow on indirect effects. These indirect effects will cause ecologically tipping points in the future through changes in competition, herbivory and predation. Evidence for indirect effects and ecological change is mostly taken from benthic ecosystems in warm temperate–tropical locations in situ that have elevated CO2. Species abundances at these locations indicate a shift away from calcifying taxa and towards non-calcareous at high CO2 concentrations. For example, lower abundance of corals and coralline algae, and higher covers of non-calcareous macroalgae, often turfing species, at elevated CO2. However, there are some locations where only minor changes, or no detectable change occurs. Where ecological tipping points do occur, it is usually at locations with naturally elevated pCO2 concentrations of 500 μatm or more, which also corresponds to just under that concentrations where the direct physiological impacts of ocean acidification are detectable on the most sensitive taxa in laboratory research (coralline algae and corals). Collectively, the available data support the concern that ocean acidification will most likely cause ecological change in the near future in most benthic marine ecosystems, with tipping points in some ecosystems at as low as 500 μatm pCO2. However, much more further research is required to more adequately quantify and model the extent of these impacts in order to accurately project future marine ecosystem tipping points under ocean acidification.\n
\n\n\n
\n\n\n
\n \n\n \n \n Krasovec, G., Renaud, C., Quéinnec, É., Sasakura, Y., & Chambon, J.\n\n\n \n \n \n \n \n Extrinsic apoptosis participates to tail regression during the metamorphosis of the chordate Ciona.\n \n \n \n \n\n\n \n\n\n\n Scientific Reports, 14(1): 5729. March 2024.\n \n\n\n\n
\n\n\n\n \n \n \"ExtrinsicPaper\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{krasovec_extrinsic_2024,\n\ttitle = {Extrinsic apoptosis participates to tail regression during the metamorphosis of the chordate \\textit{{Ciona}}},\n\tvolume = {14},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-023-48411-y},\n\tdoi = {10.1038/s41598-023-48411-y},\n\tabstract = {Abstract\n            \n              Apoptosis is a regulated cell death ubiquitous in animals defined by morphological features depending on caspases. Two regulation pathways are described, currently named the intrinsic and the extrinsic apoptosis. While intrinsic apoptosis is well studied and considered ancestral among metazoans, extrinsic apoptosis is poorly studied outside mammals. Here, we address extrinsic apoptosis in the urochordates\n              Ciona\n              , belonging to the sister group of vertebrates. During metamorphosis,\n              Ciona\n              larvae undergo a tail regression depending on tissue contraction, migration and apoptosis. Apoptosis begin at the tail tip and propagates towards the trunk as a polarized wave. We identified\n              Ci-caspase 8/10\n              by phylogenetic analysis as homolog to vertebrate caspases 8 and 10 that are the specific initiator of extrinsic apoptosis. We detected\n              Ci-caspase 8/10\n              expression in\n              Ciona\n              larvae, especially at the tail tip. We showed that chemical inhibition of\n              Ci-caspase 8/10\n              leads to a delay of tail regression, and\n              Ci-caspase 8/10\n              loss of function induced an incomplete tail regression. The specificity between apoptotic pathways and initiator caspase suggests that extrinsic apoptosis regulates cell death during the tail regression. Our study presents rare in vivo work on extrinsic apoptosis outside mammals, and contribute to the discussion on its evolutionary history in animals.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2024-04-04},\n\tjournal = {Scientific Reports},\n\tauthor = {Krasovec, Gabriel and Renaud, Cécile and Quéinnec, Éric and Sasakura, Yasunori and Chambon, Jean-Philippe},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {5729},\n}\n
\n
\n\n\n
\n Abstract Apoptosis is a regulated cell death ubiquitous in animals defined by morphological features depending on caspases. Two regulation pathways are described, currently named the intrinsic and the extrinsic apoptosis. While intrinsic apoptosis is well studied and considered ancestral among metazoans, extrinsic apoptosis is poorly studied outside mammals. Here, we address extrinsic apoptosis in the urochordates Ciona , belonging to the sister group of vertebrates. During metamorphosis, Ciona larvae undergo a tail regression depending on tissue contraction, migration and apoptosis. Apoptosis begin at the tail tip and propagates towards the trunk as a polarized wave. We identified Ci-caspase 8/10 by phylogenetic analysis as homolog to vertebrate caspases 8 and 10 that are the specific initiator of extrinsic apoptosis. We detected Ci-caspase 8/10 expression in Ciona larvae, especially at the tail tip. We showed that chemical inhibition of Ci-caspase 8/10 leads to a delay of tail regression, and Ci-caspase 8/10 loss of function induced an incomplete tail regression. The specificity between apoptotic pathways and initiator caspase suggests that extrinsic apoptosis regulates cell death during the tail regression. Our study presents rare in vivo work on extrinsic apoptosis outside mammals, and contribute to the discussion on its evolutionary history in animals.\n
\n\n\n
\n\n\n
\n \n\n \n \n Satake, H., & Sasakura, Y.\n\n\n \n \n \n \n \n The neuroendocrine system of Ciona intestinalis Type A, a deuterostome invertebrate and the closest relative of vertebrates.\n \n \n \n \n\n\n \n\n\n\n Molecular and Cellular Endocrinology, 582: 112122. March 2024.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\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{satake_neuroendocrine_2024,\n\ttitle = {The neuroendocrine system of \\textit{{Ciona} intestinalis} {Type} {A}, a deuterostome invertebrate and the closest relative of vertebrates},\n\tvolume = {582},\n\tissn = {03037207},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0303720723002733},\n\tdoi = {10.1016/j.mce.2023.112122},\n\tlanguage = {en},\n\turldate = {2024-04-04},\n\tjournal = {Molecular and Cellular Endocrinology},\n\tauthor = {Satake, Honoo and Sasakura, Yasunori},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {112122},\n}\n\n
\n
\n\n\n\n
\n\n\n
\n \n\n \n \n Taniguchi, S., Nakayama, S., Iguchi, R., Sasakura, Y., Satake, H., Wada, S., Suzuki, N., Ogasawara, M., & Sekiguchi, T.\n\n\n \n \n \n \n \n Distribution of cionin, a cholecystokinin/gastrin family peptide, and its receptor in the central nervous system of Ciona intestinalis type A.\n \n \n \n \n\n\n \n\n\n\n Scientific Reports, 14(1): 6277. March 2024.\n \n\n\n\n
\n\n\n\n \n \n \"DistributionPaper\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\n
\n
@article{taniguchi_distribution_2024,\n\ttitle = {Distribution of cionin, a cholecystokinin/gastrin family peptide, and its receptor in the central nervous system of \\textit{{Ciona} intestinalis} type {A}},\n\tvolume = {14},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-024-55908-7},\n\tdoi = {10.1038/s41598-024-55908-7},\n\tabstract = {Abstract\n            \n              The cholecystokinin (CCK)/gastrin family peptides are involved in regulation of feeding and digestion in vertebrates. In the ascidian\n              Ciona intestinalis\n              type A (\n              Ciona robusta\n              ), cionin, a CCK/gastrin family peptide, has been identified. Cionin is expressed exclusively in the central nervous system (CNS). In contrast, cionin receptor expression has been detected in the CNS, digestive tract, and ovary. Although cionin has been reported to be involved in ovulation, its physiological function in the CNS remains to be investigated. To elucidate its neural function, in the present study, we analyzed the expression of cionin and cionin receptors in the CNS. Cionin was expressed mainly in neurons residing in the anterior region of the cerebral ganglion. In contrast, the gene expressin of the cionin receptor gene\n              CioR1\n              , was detected in the middle part of the cerebral ganglion and showed a similar expression pattern to that of\n              VACHT\n              , a cholinergic neuron marker gene. Moreover,\n              CioR1\n              was found to be expressed in cholinergic neurons. Consequently, these results suggest that cionin interacts with cholinergic neurons as a neurotransmitter or neuromodulator via CioR1. This study provides insights into a biological role of a CCK/gastrin family peptide in the CNS of ascidians.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2024-04-04},\n\tjournal = {Scientific Reports},\n\tauthor = {Taniguchi, Shiho and Nakayama, Satoshi and Iguchi, Rin and Sasakura, Yasunori and Satake, Honoo and Wada, Shuichi and Suzuki, Nobuo and Ogasawara, Michio and Sekiguchi, Toshio},\n\tmonth = mar,\n\tyear = {2024},\n\tkeywords = {wrongWada},\n\tpages = {6277},\n}\n\n
\n
\n\n\n
\n Abstract The cholecystokinin (CCK)/gastrin family peptides are involved in regulation of feeding and digestion in vertebrates. In the ascidian Ciona intestinalis type A ( Ciona robusta ), cionin, a CCK/gastrin family peptide, has been identified. Cionin is expressed exclusively in the central nervous system (CNS). In contrast, cionin receptor expression has been detected in the CNS, digestive tract, and ovary. Although cionin has been reported to be involved in ovulation, its physiological function in the CNS remains to be investigated. To elucidate its neural function, in the present study, we analyzed the expression of cionin and cionin receptors in the CNS. Cionin was expressed mainly in neurons residing in the anterior region of the cerebral ganglion. In contrast, the gene expressin of the cionin receptor gene CioR1 , was detected in the middle part of the cerebral ganglion and showed a similar expression pattern to that of VACHT , a cholinergic neuron marker gene. Moreover, CioR1 was found to be expressed in cholinergic neurons. Consequently, these results suggest that cionin interacts with cholinergic neurons as a neurotransmitter or neuromodulator via CioR1. This study provides insights into a biological role of a CCK/gastrin family peptide in the CNS of ascidians.\n
\n\n\n
\n\n\n\n\n\n
\n\n\n \n\n \n \n \n \n\n
\n"}; document.write(bibbase_data.data);