Before fertilizing oocytes, haploid spermatids must extend a pseudopod which enables them to maneuver within the reproductive tract. Four mutants (
spe-8,
spe-12,
spe-27, and
spe-29 ) that prevent this process, known as spermiogenesis, are unlike other spe genes in that spermatids are defective only in virgin hermaphrodites; male sperm and self-sperm in mated animals can successfully complete spermiogenesis. To explain this phenotype, a model was created in which spermatids can begin spermiogenesis after receiving hermaphrodite- or male-derived signals. Mutations in these genes would result in an ineffective response to hermaphrodite signal, allowing sperm to differentiate only after the male signal is introduced by mating. Since
spe-12(
hc76) is likely a null mutant, we have examined its Spe phenotype in more detail. Few
spe-12(
hc76) self-sperm are rescued after mating even though mutants make normal numbers of sperm. Thus SPE-12 function is needed even when the male signal initiates spermiogenesis. As predicted,
spe-12 males are also less fertile than wild-type. This defect is subtle, however, and is detected only when males mate hermaphrodites that have self-sperm. Since mutant male sperm still outcompete wild-type self-sperm, this fertility defect may result from an increased ovulation rate (stimulated by self-sperm). Oocytes could expel
spe-12 spermatids before they complete spermiogenesis and crawl. We now favor a model in which SPE-12 functions to increase the strength of the signal. Differences in the signal itself could explain the Spe-12 phenotype: a weak hermaphrodite signal would fail to initiate spermiogenesis without SPE-12, while a stronger male signal could initiate spermiogenesis, albeit inefficiently, even in SPE-12's absence. We have cloned several of these genes to understand how they may direct spermiogenesis initiation. Though novel proteins, SPE-12 and SPE-29 each contain a single predicted transmembrane domain. SPE-12 is localized to the spermatid plasma membrane, and a SPE-12::GFP fusion localizes to spermatids as well. We are currently investigating the localization of SPE-29. As both
spe-12 and
spe-29 interact genetically with
spe-27 , perhaps all three gene products function in a signaling complex at the spermatid plasma membrane.