A molecular and genetic analysis of Caenorhabditis elegans sperm development

As animals develop, cell differentiation is controlled through the actions of numerous signaling pathways. Typically, differentiation signals lead to the regulation of various transcription factors, which in turn regulate expression of sets of genes. In certain cells incapable of realizing new gene product expression, alternate strategies must be used to control development. The transition of a C. elegans spermatid (which has no ribosomes) to a spermatozoon is one such example of an atypical developmental event. How does the signaling pathway that controls this cell differentiation differ from those whose endpoint is gene regulation? Are novel signaling mechanisms, used, or are ubiquitous signaling strategies merely adjusted to compensate for the inability of these cells to make new gene products? Here we describe progress towards understanding how the spermiogenesis initiation pathway is organized by using two distinct approaches. We have utilized a classical genetics approach to identify and characterize mutants with defects in sperm activation. The phenotypic and molecular characterization of two genes, the previously described spe-12 and the newly identified spe-29, are described. Based on the phenotypes of these mutants, we present a model for sperm activation in which a weak hermaphrodite-derived or strong male-derived signal can stimulate sperm activation. Additionally, we describe a microarray-based large-scale screen for genes expressed during spermatogenesis. Over 450 genes expressed only during spermatogenesis in the adult were identified. Surprisingly, almost none of these genes are present on the X chromosome, suggesting a difference in transcription between autosomes and the sex-chromosome during spermatogenesis. Characterization of select sperm genes with predicted molecular functions will further our understanding of sperm development and activation