Apoptosis promotes fertility in C. elegans by maintaining functional germline morphology

Programmed cell death (apoptosis) during oogenesis is conserved across metazoans and linked to regulation of oocyte number and quality. In oogenic germlines, the removal of developing oocytes by apoptosis ensures that oocytes do not contain DNA damage or multiple nuclei. Beyond this chromatin-quality control assurance role, it was unknown how apoptosis contributes to oocyte quality. We used the nematode Caenorhabditis elegans (C. elegans) to study the consequences of loss of apoptosis on oogenesis. Blocking apoptosis reduced fecundity in hermaphrodites at peak fertility and caused germline architectural defects such as abnormal rachis morphology and perturbed the arrangement and distribution of oogenic germline compartments. We posit that the defects associated with the loss of germline apoptosis arise due to lack of sufficient space for normal oogonia growth. In support of this idea, oocytes and embryos are abnormally small and exhibit low viability in animals unable to execute apoptosis. These findings suggest that in addition to preventing ploidy defects during oogenesis, apoptosis contributes to fertility by preserving homeostatic germline structure required for the fidelity of oogenesis. Summary StatementBlocking apoptosis during oogenesis disrupts germline structure over time, causing morphological defects and infertility, highlighting the role of apoptosis in maintaining syncytial architecture and reproductive function.