Our goal is to understand how different cell types regulate programmed cell death in C. elegans . Toward this end, we are defining the genes necessary for Hermaphrodite-Specific Neuron (HSN) death. The HSNs are a pair of motor-neurons that are required for egg-laying. The HSNs die by programmed cell death in males, presumably in response to masculine signals from the sex determination pathway. The HSNs also die in hermaphrodites carrying gain-of function alleles of the
egl-1 gene. Hermaphrodites lacking HSNs are defective in egg-laying (Egl), but are viable and display no pleiotropic defects. Thus,
egl-1(gf) provides a good background to identify mutations in genes that are specifically required for HSN death, as restoration of HSN function must be achieved by blocking its death. In a screen for mutants that revert the egg-laying defect of
egl-1(
n1084) , we isolated two mutations,
op181 IV and
op166 X, that are required for HSN death, but not, as far as we can tell, any other cell death. In addition to suppressing HSN death,
op181 and
op166 have a common set of pleiotropic defects including uncoordinated movement, lethality with a terminal Clr phenotype, egg-laying defects and male mating defects. We speculate that
op181 and
op166 are mutations in genes required for complete differentiation in the nervous system.