| Abstract |
Oocyte production, maturation and ovulation must be coordinated with sperm availability for successful fertilization. In C. elegans this coordination involves signals from the sperm to the oocyte and somatic gonad, which stimulate maturation and ovulation. We have found that the C. elegans early growth response factor family member EGRH-1 inhibits oocyte maturation and ovulation until sperm are available. In the absence of sperm, egrh-1 mutants exhibit derepressed oocyte maturation marked by MAPK activation and ovulation. egrh-1 mutants exhibit ectopic oocyte differentiation in the distal gonadal arm and accumulate abnormal and degraded oocytes proximally. These defects result in reduced brood size and partially penetrant embryonic lethality. We have found that endogenous EGRH-1 protein and an egrh-1::gfp reporter gene are expressed in the sheath and distal tip cells of the somatic gonad, the gut and other non-gonadal tissues, as well as in sperm, but expression is not observed in oocytes. Results of tissue-specific egrh-1(RNAi) experiments and genetic mosaic analyses revealed that EGRH-1 function is necessary in the soma and, surprisingly, this function is required in both the gut and the somatic gonad. Based on transformation rescue experiments we hypothesize that EGRH-1 in the somatic gonad inhibits oocyte maturation and ovulation.
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