In C. elegans, male sperm compete with hermaphrodite self sperm, resulting in the preferential use of male sperm. This differential fertilization success, termed male precedence, is nearly absolute. Evidence indicates that male precedence relies on intrinsic differences between male and hermaphrodite sperm. One such difference is that males have larger sperm than that of the hermaphrodite. While larger sperm size is correlated with faster crawling speeds, size does not correlate perfectly with velocity, suggesting that additional factors contribute to male precedence. By identifying sperm-specific gene products required for male precedence, we seek to understand the cellular and molecular mechanisms important for cell competition. Mutations in the kinase gene F37E3.3 lead to reduced male precedence and migration defects. While wild-type male sperm migrate rapidly to the spermathecae, mutant sperm slowly accumulate in the spermathecae. However, F37E3.3 defects are dependent on the competitive context, as mutant sperm are functional by several criteria. Critically, mutant males and hermaphrodites have normal fertility. In addition, mutant sperm appear grossly normal with properly polarized sperm structures, and their in vitro velocity is indistinguishable from the wild type. The mutant sperm migration defect is ameliorated in
spe-8 hermaphrodites, which lack activated sperm and contain unfertilized oocytes. Thus, the hermaphrodite reproductive environment likely plays a role in the aberrant mutant sperm migration behaviors. Currently, we are testing two models; that unfertilized oocytes might provide a better substrate for adhesion for mutant sperm, or the presence of activated hermaphrodite sperm might have an inhibitory effect on male sperm. F37E3.3 is expressed in and displays a punctate pattern that is restricted to the cell body, but it does not associate with known sperm structures. Notably, mutant spermatids are the same size as wild-type, suggesting that mechanisms in addition to size contribute to male sperm precedence. To date, F37E3.3 is the only gene identified that specifically affects C. elegans male precedence and its characterization likely will reveal a novel mechanism for sperm competition.