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• W1571857400 abstract "Programmed cell death plays a central role in the development of most multicellular animals. During the development of Caenorhabditis elegans, a total of 1090 cells are generated, 131 of which are destined to die. Genetic studies focusing on the control of the fate of these 131 cells revealed an evolutionary conserved set of genes essential for all programmed cell deaths in C. elegans. In a cell undergoing apoptosis, the BH3-only domain protein EGL-1 binds to the CED-9–CED-4 complex on the outer mitochondrial membrane resulting in the release of CED-4, which in turn activates the effector caspase CED-3. These at the time pioneering findings established C. elegans as a prime model system to study apoptosis, a system that still today provides a stage for new inspiring science, such as studies on C. elegans apoptotic cell clearance and on deoxyribonucleic acid (DNA) damage-induced apoptosis. Key concepts: Caenorhabditis elegans as a model organism has been introduced by Sidney Brenner in the 1960s. The complete C. elegans cell lineage was described in 1983 by John Sulston. The cell lineage in C. elegans is invariant: during the development of an animal, a total of 1090 cells are generated, 131 of which are destined to die. The basis for analysing programmed cell death in C. elegans was delineation of the complete cell lineage. There are three waves of programmed cell death in C. elegans: a first wave can be observed in embryos, the second smaller wave during the second larval stage, whereas the third wave occurs in the adult germline. Germline apoptosis is a stochastic process in which half of the germ cells undergo apoptotic cell death. CED-4 and CED-3 are killer proteins essential for all programmed cell deaths in C. elegans. CED-9 is homologous to Bcl-2 and protects from cell death. In a cell undergoing apoptosis, the BH3-only domain protein EGL-1 inhibits CED-9 from inhibiting CED-4. The central cell death pathway is conserved through evolution; homologues of EGL-1, CED-9, CED-4 and CED-3 are present in mammals, where they control the mitochondrial pathway for apoptosis. Apoptotic cell clearance is controlled via two partially redundant intracellular signalling cascades that converge at the Rac1 homologue CED-10. DNA damage-induced germline apoptosis is triggered by a genomic integrity checkpoint and activates a pathway including the p53 homologue CEP-1." @default.
• W1571857400 created "2016-06-24" @default.
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• W1571857400 date "2009-12-15" @default.
• W1571857400 modified "2023-09-23" @default.
• W1571857400 title "Cell Death inC. elegans" @default.
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• W1571857400 doi "https://doi.org/10.1002/9780470015902.a0021563" @default.
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