The Role of sgd-8 in the Control of Oocyte Meiotic Maturation in Caenorhabditis elegans

Abstract

Oocyte meiotic maturation is a highly conserved biological process required for sexual reproduction. In human females, the frequency of meiotic errors increases with maternal age, and these mistakes can lead to miscarriage, infertility, or Down Syndrome. At present, C. elegans is the only genetic model organism in which we can observe oocyte development, meiotic maturation, and ovulation in the intact living animal. In C. elegans, major sperm signal (MSP) is a hormone used to promote oocyte meiotic maturation. A receptor of this signal, VAB-1 (variable abnormal morphology)/Eph receptor, functions as part of a sperm-sensing control mechanism that regulates oocyte meiotic maturation. The gsa-1 gene encodes the stimulatory G protein alpha subunit, is necessary and sufficient to promote oocyte meiotic maturation. A large-scale forward genetic screen from prior work identified mutations that suppress the requirement of gsa-1 for oocyte meiotic maturation effect. One of the mutations identified, sgd-8 (suppressor of gsa-1 maturation defect) is represented by five alleles. Preliminary studies show that sgd-8 mutants are sensitive to somatic RNAi, but resistant to RNAi in the germline. To better understand how sgd-8 functions as a regulator of oocyte meiotic maturation, we are conducting genetic and phenotypic analysis of sgd-8 mutants. Using snip-SNP mapping, sgd-8 was mapped to LG III. Currently, we are fine mapping sgd-8 to an interval for positional cloning, and have successfully narrowed the interval.