The normal program of early embryonic development is initiated when an oocyte is fertilized by a sperm. The mechanism by which sperm activate oocytes and the role of sperm components in this process and in later stages of embryogenesis are not understood. This project takes a combined genetic and molecular approach to studying this problem, using the nematode Caenorhabditis elegans as a model system. The PI has already identified a gene that encodes a sperm-supplied product that is required for initiation of the correct program of early embryonic development in C. elegans. Mutations in this gene, called spe-11, result in paternal-effect embryonic lethality: wild-type oocytes, when fertilized by sperm from mutant worms, undergo very abnormal early development and die. This is not due to the presence of a "poisonous product" in mutant sperm but to reduced levels or absence of wild-type product. Thus, wild-type spe-11 product participates, either directly or indirectly, in initiating the normal program of early development in C. elegans. This project has two major aims: 1) To clone and molecularly characterize the spe-11 gene, and localize the spe-11 gene product in sperm and newly fertilized embryos. 2) To carry out screens for additional paternal-effect embryonic-lethal mutations, which will identify other genes that encode sperm-supplied factors required for normal embryo development. This effort will complement the wealth of information on oocyte factors and will begin to define the sperm's contributions to early embryogenesis.
