Spermatid activation is required in order to initiate the quest for oocyte fertilization. Activation may be initiated by TRY-5 in males and by zinc in males and hermaphrodites. The zinc activation signal is transduced through the
spe-8 group genes (
spe-8,
spe-12,
spe-19,
spe-27, and
spe-29). A mutation in any one of these genes results in sterility. A large suppressor screen recovered numerous mutations that suppress
spe-27(
it132ts) sterility. The vast majority of the suppressor mutations restore fertility by bypassing the need for an activation signal altogether, because the sperm activate prematurely. Results from the suppressor allele
spe-47(
hc198) has shown that this mutation is a recessive suppressor of
spe-27(
it132ts), but it has a semidominant sperm defective phenotype on its own. Further,
spe-47(
zq19), a molecular null, results in only a small reduction of fertility. We are investigating the possibility that redundant gene function masks the null
spe-47 allele. A single paralog to
spe-47 exists in the C. elegans genome: Y48B6A.5, and RT-PCR revealed that it is a sperm gene. Both
spe-47 and Y48B6A.5 contain an MSP domain in their C-terminus. SPE-47 is expressed during spermatogenesis in primary spermatocytes, where it appears to interact with FB-MOs. Preliminary analysis of Y48B6A.5 suggests a similar pattern of expression. A fecundity analysis of a strain harboring the
ttTi4488 Mos1 insertion in Y48B6A.5 shows no dramatic decrease in fertility, similar to what we have found with the
spe-47 null mutation. Interestingly, a double
spe-47(
zq19);
ttTi4488 mutant shows little if any effect on fertility. We are now focusing on the suppressor mutation, as it appears to be a gain of function. In a
ttTi4488 background, the
spe-47(
zq19) mutation results in near sterility. We created an equivalent mutation to
spe-47(
hc198) in Y48B6A.5. This mutation appears to suppress the
spe-8 group gene,
spe-19, likely also due to premature activation. We will present data for various combinations of knockout and suppressor alleles in both genes. Our results suggest that loss of both gene products is without major effects on spermatogenesis, but the suppressor mutations cause premature sperm activation through an as yet unknown gain of function.