Apoptosis promotes fertility in Caenorhabditis elegans by maintaining functional germline morphology
TL;DR
Oocytes and embryos are abnormally small and exhibit low viability in animals unable to execute apoptosis, suggesting that, in addition to preventing ploidy defects during oogenesis, apoptosis contributes to fertility by preserving the homeostatic germline structure required for the fidelity of oogenesis.
Abstract
ABSTRACT 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 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 arrangement and distribution of oogenic germline compartments. Our results suggest that the loss of germline apoptosis arises due to lack of sufficient space for, and reduced cytoplasmic flows into, developing oogonia. 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 the homeostatic germline structure required for the fidelity of oogenesis.