TY  - CHAP
T1  - Germ cell apoptosis and DNA damage responses
A1  - Bailly,Aymeric
A1  - Gartner,Anton
AU  - Bailly,Aymeric
AU  - Gartner,Anton
PB  - Springer
CY  - New York
PY  - 2013
Y1  - 2013
N2  - In the past 12 years, since the first description of C. elegans germ cell apoptosis, this area of research rapidly expanded. It became evident that multiple genetic pathways lead to the apoptotic demise of germ cells. We are only beginning to understand how these pathways that all require the CED-9/Bcl-2, Apaf-1/CED-4 and CED-3 caspase core apoptosis components are regulated. Physiological apoptosis, which likely accounts for the elimination of more than 50% of all germ cells, even in unperturbed conditions, is likely to be required to maintain tissue homeostasis. The best-studied pathways lead to DNA damage-induced germ cell apoptosis in response to a variety of genotoxic stimuli. This apoptosis appears to be regulated similar to DNA damage-induced apoptosis in the mouse germ line and converges on p53 family transcription factors. DNA damage response pathways not only lead to apoptosis induction, but also directly affect DNA repair, and a transient cell cycle arrest of mitotic germ cells. Finally, distinct pathways activate germ cell apoptosis in response to defects in meiotic recombination and meiotic chromosome pairing. © 2013 Springer Science+Business Media New York.
AB  - In the past 12 years, since the first description of C. elegans germ cell apoptosis, this area of research rapidly expanded. It became evident that multiple genetic pathways lead to the apoptotic demise of germ cells. We are only beginning to understand how these pathways that all require the CED-9/Bcl-2, Apaf-1/CED-4 and CED-3 caspase core apoptosis components are regulated. Physiological apoptosis, which likely accounts for the elimination of more than 50% of all germ cells, even in unperturbed conditions, is likely to be required to maintain tissue homeostasis. The best-studied pathways lead to DNA damage-induced germ cell apoptosis in response to a variety of genotoxic stimuli. This apoptosis appears to be regulated similar to DNA damage-induced apoptosis in the mouse germ line and converges on p53 family transcription factors. DNA damage response pathways not only lead to apoptosis induction, but also directly affect DNA repair, and a transient cell cycle arrest of mitotic germ cells. Finally, distinct pathways activate germ cell apoptosis in response to defects in meiotic recombination and meiotic chromosome pairing. © 2013 Springer Science+Business Media New York.
UR  - http://www.scopus.com/inward/record.url?partnerID=yv4JPVwI&eid=2-s2.0-84867539316&md5=8bae59a1d8cfed2a1bcee4c0386522d9
U2  - 10.1007/978-1-4614-4015-4
DO  - 10.1007/978-1-4614-4015-4
M1  - Other chapter contribution
SN  - 9781461440147
VL  - 757
BT  - Germ Cell Development in C. elegans
T2  - Germ Cell Development in C. elegans
A2  - Schedl,Tim
ED  - Schedl,Tim
T3  - Advances in Experimental Medicine and Biology
T3  - en_GB
SP  - 249
EP  - 276
ER  -