Cytokinesis, the division of the plasma membrane that sequesters newly replicated nuclei into separate cells, is a fundamental biological process that remains poorly understood. We have yet to uncover in any detail what signals induce plasma membrane constriction at the point of division, how the membrane is anchored to the actin cytoskeleton or how the nascent daughter cells resolve their membranes. To study cytokinesis, we have identified in the nematode Caenorhabditis elegans a maternal effect, recessive mutation within a gene we call odd-1. Embryos from mothers homozygous for a mutation in odd-1 (allele designation or36) undergo what appears to be a normal set of organizational events during most of their first cell cycle. At the end of mitosis, however, the mutant embryos invariably fall to complete cytokinesis. We propose to continue our analysis of the odd-1 mutant phenotype, to isolate more mutant alleles of odd-1 and to clone the wild-type odd-1 gene. Our preliminary analysis suggests that a better understanding of the odd-1 mutant may contribute significantly towards understanding the molecular mechanisms that execute cytokinesis. Specifically, understanding why cytokinesis is blocked in odd-1 mutant embryos may help reveal how the contractile ring is physically associated with the plasma membrane, the mechanism of ring constriction or how the actin contractile ring is signaled to begin separation of the membrane. Effective interaction between the cytoskeleton and plasma membrane is essential for the correct functioning and well being of many cell types and ultimately for the health of the individual. We regard the odd-1 mutant as an exciting chance to gain information on membrane/cytoskeletal interactions.
