The Caenorhabditis elegans male and hermaphrodite nervous systems display sexually dimorphic development characterized, in part, by the presence of 8 hermaphrodite-specific neurons and 89 male-specific neurons. We are interested in identifying the genes and molecular mechanisms that govern sex-specific neural development in C. elegans. Through a mutagenesis screen using a pkd-2::GFP reporter to label male-specific neurons, we recovered several mutants that display defects in sex-specific neural development. Males carrying the sm129 mutation lack pkd-2::GFP expression in the male-specific CEM neurons that are involved in mate finding. Genetic epistasis experiments suggest that CEM neurons are improperly specified or differentiated. We cloned the sm129 mutation and determined that it is an allele daf-19 based on three pieces of evidence: (1) RNAi of daf-19 phenocopies sm129, (2) sm129 fails to complement a daf-19 null mutation, and (3) we found a mutation in daf-19 that likely affects splicing. We are also testing to see if sm129 mutants can be rescued by adding a wild type copy of daf-19. daf-19 encodes an RFX transcription factor that activates genes required for sensory cilia function in ciliated neurons such as the CEMs. daf-19 null mutants lack all sensory cilia, have sensory defects, and display a constitutive dauer phenotype (worms enter an alternative part of the lifecycle associated with starvation survival). We are currently investigating how this mutation affects ciliated neurons such as CEMs but does not affect dauer formation.