Abstract

Six independent mutations in the Caenorhabditis elegans spe-26 gene cause sterility in males and hermaphrodites by disrupting spermatogenesis. Spermatocytes in mutants with the most severe alleles fail to complete meiosis and do not form haploid spermatids. Instead, these spermatocytes arrest with missegregated chromosomes and mislocalized actin filaments, endoplasmic reticulum and ribosomes. In spite of this arrest some of the nuclei and the organelles that normally transport sperm-specific components to the spermatid mature as if they were in spermatids. The spe-26 gene is expressed throughout the testis in both spermatogonial cells and spermatocytes. It encodes a 570-amino-acid polypeptide, which contains five tandem repeat motifs, each of approximately 50 amino acids. These repeats are similar in sequence to repeats in the Drosophila kelch protein, in the invertebrate sperm protein scruin that cross-links actin filaments, as well as in the mouse and pox virus proteins. The functional importance of these repeat motifs is shown by the fact that five of the spe-26 mutations are in the tandem repeats, and one of the most severe mutations is a substitution in a highly conserved glycine. These results suggest that spe-26 encodes a cytoskeletal protein, perhaps actin binding, which is necessary to segregate the cellular components that form haploid spermatids.