spe-29 encodes a small predicted membrane protein required for the initiation of sperm activation in Caenorhabditis elegans

Caenorhabditis elegans spermatidis complete a dramatic morphogensis to craw ling spermatozoa in the absence of an actin- or tubulin-based cytoskeleton and without synthesizing new gene products. Mutations in three genes (spe-8 , spe-12, and spe-27) prevent the initiation of this morphogensis, termed a ctivation. Males with mutations in any of these genes are fertile. By contr ast, mutant hermaphrodites are self-sterile when unmated due to a failure i n spermatid activation. Intriguingly, mutant hermaphrodites are self-functi onal spermatozoa and become self-fertile upon mating, suggesting that sperm atids can be activated by male seminal fluid. Here we describe a mutation i n a fourth gene, spe-29, which mimics the phenotype of spe-8, spe-12, adn s pe-27 mutants. spe-29 sperm are defective in the initiation of hermaphrodit e sperm activation, yet they maintain the ability to complete the morphogen etic rearrangements that follow. Mutant alleles of spe-12, spe-27, and spe- 29 exhibit genetic interactions that suggest that the wild-type products of spe-29 gene, which is expressed specifically in the sperm-producing germ l ine and is predicted to encode a small, novel transmembrane protein.