As women age, the quality and quantity of their oocytes declines, resulting in fewer pregnancies and an increased chance of having a child with birth defects. We are using the nematode C. elegans to study how oocyte quality is regulated during aging. To assay quality, we use
fog-2(
q71) females mated at various ages, and determine the fraction of oocytes that produce viable eggs after fertilization. Our previous results showed that oocyte quality declines in older nematodes, as in humans. Furthermore, apoptosis helps alleviate this problem, since mutations in
ced-3 and
ced-4 prematurely lower oocyte quality during aging. Surprisingly, a loss-of-function mutation in
egl-1, which normally prevents germ cells from undergoing cell death in response to DNA damage, appeared to improve oocyte quality in older animals. Normally, CEP-1 acts through EGL-1 and CED-13 to control CED-9 activity and regulate germ cell deaths. As expected, we found that EGL-1 promotes oocyte quality in young irradiated animals. However,
egl-1 mutants,
ced-13 mutants and
egl-1;
ced-13 double mutants produced high quality oocytes when old, which implies that EGL-1 and CED-13 are harmful to oocytes in older animals. Furthermore,
egl-1(lf) mutations lowered the number of dying germ cells in older animals. Finally the harmful effects of EGL-1 depended on apoptosis, since
ced-3 mutants and
ced-3;
egl-1 double mutants behaved similarly. Thus, we suspect that EGL-1 lowers the quality of oocytes in older animals by inappropriately stimulating apoptosis. We also noted that
egl-1(lf) animals reproduced for a longer period of time than wild-type animals. Since oocyte quality declines with age, it might be influenced by genes that regulate lifespan. To test this idea, we studied
daf-2(
e1370ts) mutants and found that they showed improved oocyte quality when old. Furthermore, the effect of
daf-2 on oocyte quality depended on
daf-16 but was not affected by mutations in
ced-3. Thus, we suspect that selection optimized the production of high quality oocytes in young animals, during their peak reproductive period. Genes like
egl-1 and
ced-13, which control some germ cells death, and
daf-2, which regulates the response to certain forms of stress, might not have optimal activity in older females.