Prior to fertilization, C. elegans oocytes arrest in meiosis, and they require signals from both sperm and the somatic gonad to undergo maturation and ovulation. In the absence of sperm, wild-type animals continue to produce oocytes that accumulate in the proximal gonad and do not activate a MAPK involved in maturation. We have found the zinc-finger protein C27C12.2 regulates oocyte maturation and ovulation. C27C12.2 shows high sequence similarity to mammalian EGR proteins and we have therefore named the C27C12.2 gene
egrh-1 (early growth response factor homology).
egrh-1(
tm1736) mutant hermaphrodites accumulate degraded and abnormal oocytes in the proximal and distal gonadal arms, resulting in reduced brood size and partially penetrant embryonic lethality. In the absence of sperm,
egrh-1 mutants exhibit constitutive ovulation and MAPK activation in proximal oocytes.
egrh-1 mutant oocyte defects can be rescued by transformation with cosmid C27C12 and are phenocopied by
egrh-1(RNAi), indicating
egrh-1(
tm1736) is a loss-of-function allele. Previous analyses suggest
egrh-1 mRNA is widely expressed, with strong expression in the hermaphrodite gonad. We have used an EGRH-1 antibody to examine protein expression in the gonad and found specific staining in the somatic distal tip cell and sheath cells, as well as more variable staining in sperm.
egrh-1(RNAi) in a strain resistant to somatic RNAi produced only weak oocyte defects, indicating
egrh-1 expression in the soma is sufficient for ovulation and oocyte maturation. In
egrh-1 mutants, both wild-type and
egrh-1</I> mutant sperm are not efficiently recruited to the spermatheca, suggesting EGRH-1 is also required for gonadal signals recruiting sperm. We hypothesize EGRH-1 regulates genes in the somatic gonad controlling ovulation, oocyte maturation, and sperm recruitment.