Germ cell apoptosis and DNA damage responses

Aymeric Bailly, Anton Gartner

    Research output: Chapter in Book/Report/Conference proceedingOther chapter contribution

    51 Citations (Scopus)


    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.
    Original languageEnglish
    Title of host publicationGerm Cell Development in C. elegans
    EditorsTim Schedl
    Place of PublicationNew York
    Number of pages28
    ISBN (Electronic)9781461440154
    ISBN (Print)9781461440147
    Publication statusPublished - 2013

    Publication series

    NameAdvances in Experimental Medicine and Biology
    ISSN (Print)0065-2598


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