Germline survival and apoptosis.

Anton Gartner, Peter R Boag, T Keith Blackwell
Author Information
  1. Anton Gartner: Wellcome Trust Centre for Gene Regulation and Expression, University of Dundee, Dundee, DD1 5EH, UK. a.gartner@dundee.ac.uk

Abstract

Germline apoptosis shares with somatic apoptosis a reliance on key components of the core apoptotic machinery, including CED-3 and CED-4. However, germline apoptosis differs from somatic apoptosis in its regulation. Whereas somatic apoptosis is developmentally programmed by cell lineage, germline apoptosis occurs as part of an oogenesis program. One category of germline apoptosis, dubbed "physiological" germline apoptosis, reduces the number of cells that complete oogenesis, and is independent of the BH3-only apoptosis effecter EGL-1. A second category, termed "stress-induced" germline apoptosis, is triggered by a genomic integrity checkpoint. Some mechanisms that are monitored by this DNA-damage checkpoint are also involved in germ cell "immortality," or preservation of a continuous germ cell lineage over successive generations. In addition, exposure to certain environmental insults or pathogens induces germ cell apoptosis. Here we will review the mechanisms that control each of the pathways leading to germ cell apoptosis and discuss their functional significance. Germline apoptosis is an integral part of oogenesis in many animals, including humans. Because many of the regulators of C. elegans germline apoptosis are conserved, we suggest that this nematode provides a valuable model for understanding controls of germline apoptosis more broadly.

MeSH Term

Animals
Apoptosis
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Cell Survival
DNA Damage
Germ Cells
Humans
Meiosis
Oogenesis
Tumor Suppressor Protein p53

Chemicals

CEP-1 protein, C elegans
Caenorhabditis elegans Proteins
Tumor Suppressor Protein p53

Word Cloud

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