Abstract

Hermaphrodites with mutations in the spe-27 gene are self-sterile, laying only unfertilized eggs; mutant males are fertile. Hermaphrodites make spermatids that fail to activate to crawling spermatozoa so passing oocytes sweep them out of the spermatheca. These spermatids do activate and produce self-progeny if young mutant hermaphrodites are mated by fertile (or sterile) males. Spermatids isolated from either mutant males or hermaphrodites initiate activation in vitro when treated with proteases, but then arrest with spiky membrane projections that resemble those of a normal intermediate in pseudopod formation. These phenotypes are identical to spe-8 and spe-12 mutants. They can be explained if males and hermaphrodites have distinct pathways for spermatid activation, and these three genes are necessary only for the hermaphrodite pathway. Consistent with this model, when spe-27 mutant male spermatids without seminal fluid are artificially inseminated into hermaphrodites, they fail to activate. The spe-27 gene has been isolated, sequenced and its regulatory regions identified. The sequence predicts a 131 amino acid polypeptide that has no striking structural motifs and no resemblance to known proteins. Two of the mutations in spe-27 alter mRNA splicing; a third mutation is a temperature-sensitive missense mutation.