Hermaphrodites do not need males to reproduce and may encounter them rarely, so it is advantageous for males to ensure that any rendezvous with a hermaphrodite results in reproductive success. When a male mates with a hermaphrodite, he transfers spermatids, which become activated and crawl to the spermatheca where they displace self sperm and preferentially fertilize the hermaphrodite's eggs. How do male sperm win? We are interested in how sperm functions (e.g., activation, motility, or interactions with the hermaphrodite reproductive tract and oocytes) are modulated to enhance males' ability to reproduce.We are screening for mutant males that fail to show precedence in crosses to hermaphrodites. We cross males from mutagenized
him-5 lines to
spe-8;
dpy-4 tester hermaphrodites, which cannot activate their own spermatids and thus produce no progeny prior to mating. Matings with wild-type males result in nearly 100% cross progeny; we select lines for which testers produce an increased fraction of self progeny. Using this screen, we can identify both mutations that affect male sperm precedence and mutations that affect spermatogenesis specifically in males.For one class of mutants, male sperm appear morphologically normal but are used inefficiently. These mutants may define factors important for sperm competition. For the
me69 mutant, hermaphrodites have normal brood sizes, suggesting that
me69 hermaphrodite sperm are used efficiently in the absence of competition. We are using mitotracker dye to label male sperm so that their behavior within hermaphrodites can be tracked. Using this assay, it appears that
me69 sperm accumulate more slowly in spermathecae than do wild-type sperm. Although this delay may not fully explain the precedence defect, these data do indicate that
me69 may be involved in some aspect of sperm motility or targeting to the spermathecae.A second class of mutants activates sperm inappropriately within the male gonad. Whereas wild-type virgin males accumulate unactivated spermatids,
me66 males contain activated sperm, which can crawl throughout the gonad.
me66 males mate at normal rates but most fail to transfer sperm. Occasionally, sperm are transferred, and these migrate to the spermatheca. Our results suggest that reproductive success in males depends on inhibiting sperm activation until after transfer. We are testing whether premature activation in
me66 is dependent on other spermiogenesis genes. We have obtained cosmid rescue of the
me66 mutant and hope to report on the molecular identity of the
me66 gene at the meeting.