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WBPicture0000013091 | Description | Figure 2. Regulation of germ cell apoptosis. At least two distinct pathways of germ cell apoptosis function in C. elegans. Physiological apoptosis is cep-1-independent and a normal feature of oogenesis. The frequency of cep-1-independent germ cell apoptosis increases in response to various cytoplasmic stresses (oxidative, heat, osmotic, starvation). It is not clear whether this increase involves the same triggering mechanism as physiological apoptosis. In each case, these apoptotic events depend upon Ras/MAP-kinase signaling. CEP-1-dependent apoptosis is induced by a DNA damage or chromosomal integrity checkpoint. Rb and E2F transcription factor subunits promote physiological cell death, and appear to function downstream of or in parallel to CEP-1 in the DNA damage response. Pathogen-induced germ cell apoptosis is arbitrarily shown as acting directly on EGL-1, because it has not been determined whether CEP-1 is involved. Physiological and DNA damage germ cell apoptosis pathways are suppressed by the PAX-2 and EGL-38 Pax-family proteins, which increase transcription of the anti-apoptotic protein CED-9. | |||
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Name | FigB.jpg | ||||
Depict | WBProcess | WBbiopr:00000104 | |||
Gene (16) | |||||
Acknowledgment | Template | From: <Journal_URL> <Article_URL>. Copyright <Publication_year>. | |||
Publication_year | 2008 | ||||
Article_URL | DOI | id | 10.1895/wormbook.1.145.1 | ||
Journal_URL | WormBook | ||||
Publisher_URL | Caltech | ||||
Reference | WBPaper00032172 |