Loss of PGL-1 and PGL-3, members of a family of constitutive germ-granule components, promotes germline apoptosis in C. elegans.

In Caenorhabditis elegans, the mechanisms regulating germline apoptosis remain largely unknown, except for the core machinery. Here, we found that mutants of pgl-1 and pgl-3, encoding members of a family of constitutive protein components of germline-specific P granules, showed increased germline apoptosis under both physiological and DNA-damaged conditions. We also found that the number of germ cells that lost PGL proteins increased significantly following UV irradiation, and that only those PGL-absent germ cells were selectively engulfed by gonadal sheath cells in adult hermaphrodite gonads. We further revealed that CEP-1, the p53 homolog, and the caspase CED-3 promoted elimination of PGL-1 from germ cells following UV irradiation. Furthermore, protein levels of CED-4, the Apaf-1 homolog, and cytoplasmic translocation of SIR-2.1, a Sirtuin homolog, significantly increased in pgl mutants and increased even more following UV irradiation. CED-4 and SIR-2.1 were essential for high levels of germline apoptosis in pgl mutants. We conclude that PGL proteins suppress excessive germline apoptosis by repressing both the protein levels of CED-4 and the cytoplasmic translocation of SIR-2.1. Our study has revealed new roles for PGL-1 and PGL-3 in the control of germline apoptosis.

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