In C. elegans, both sexes make sperm, but males do it better. Male sperm are used preferentially if available. While male sperm precedence has been demonstrated to be due to intrinsic superiority of the cells themselves and correlates with the larger size of male sperm, the molecular mechanisms underlying this phenomenon are not understood. We are interested in how sperm functions are modulated to ensure a male's reproductive success. In this context, we are focusing on two questions: how do male sperm become motile, and how is sperm motility linked to sperm competition? Male and hermaphrodite sperm acquire motility during a process known as activation, which is differentially regulated in the two sexes. While hermaphrodite sperm are activated shortly after they complete meiosis, male sperm are only activated after transfer. We have identified a protease, TRY-5, which is likely to function as the male sperm activator.
try-5 males are defective for transfer of activator, and a TRY-5::GFP fusion is expressed in the vas deferens and transferred to hermaphrodites during copulation. However,
try-5 is not absolutely required for male fertility, perhaps because hermaphrodite activator can compensate in its absence. In our studies of sperm competition, we have identified a mutant,
me69, which shows reduced male precedence and altered patterns of sperm migration to the spermathecae. The precedence defect depends on the competitive environment:
me69 male sperm compete better against hermaphrodite sperm from
me69 than those from the wild type. Unmated
me69 hermaphrodites have normal brood sizes, suggesting that mutant sperm are fully functional when they do not need to compete. Sperm size does not appear to be altered in
me69 males. Currently we are using a whole genome sequencing and candidate rescue approach to try to identify the
me69 gene.