spe-29 Encodes a Small Predicted Membrane Protein Required for the Initiation of Sperm Activation in Caenorhabditis elegans

Corresponding author: Samuel Ward, MCB Department, University of Arizona, Life Sciences South No. 452, Tucson, AZ 85721., samward{at}u.arizona.edu (E-mail)

Communicating editor: R. K. HERMAN

Caenorhabditis elegans spermatids complete a dramatic morphogenesis to crawling 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 morphogenesis, termed activation. Males with mutations in any of these genes are fertile. By contrast, mutant hermaphrodites are self-sterile when unmated due to a failure in spermatid activation. Intriguingly, mutant hermaphrodites form functional spermatozoa and become self-fertile upon mating, suggesting that spermatids can be activated by male seminal fluid. Here we describe a mutation in a fourth gene, spe-29, which mimics the phenotype of spe-8, spe-12, and spe-27 mutants. spe-29 sperm are defective in the initiation of hermaphrodite sperm activation, yet they maintain the ability to complete the morphogenetic rearrangements that follow. Mutant alleles of spe-12, spe-27, and spe-29 exhibit genetic interactions that suggest that the wild-type products of these genes function in a common signaling pathway to initiate sperm activation. We have identified the spe-29 gene, which is expressed specifically in the sperm-producing germ line and is predicted to encode a small, novel transmembrane protein.

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				P. J. Muhlrad and S. Ward Spermiogenesis Initiation in Caenorhabditis elegans Involves a Casein Kinase 1 Encoded by the spe-6 Gene Genetics, May 1, 2002; 161(1): 143 - 155. [Abstract] [Full Text] [PDF]