In order to generate two functionally distinct sexes, sex-determination mechanisms must work in conjunction with generic developmental pathways to bring about unique changes in cellular differentiation and morphogenesis. How sex-determining factors generate dimorphic features from an otherwise identical cellular lineage is poorly understood. An example of this is ray neurogenesis in C. elegans. In males, the posterior seam cells give rise to neural precursors that generate rays, sensory organs required for mating. The DM gene mab-3 and the Hox gene mab-5 function in the male seam to activate the proneural gene lin-32, which triggers the ray sublineage. However, the activity of these genes does not appear to be restricted to males, making it unclear why ray neurogenesis is sex-specific. In order to better understand how the sexual identity of the seam affects ray neurogenesis, we used seam-specific promoters to drive expression of activators or inhibitors of the master sex-determination regulator tra-1. This cell-autonomously “flips” the state of the sex-determination pathway, genetically reversing seam sexual identity. Interestingly, we found that masculinization of the hermaphrodite seam resulted in the development of ray neurons as well as a loss of alae formation in the posterior of the animal, indicating that “maleness” in the seam is sufficient to bring about ray neurogenesis. Masculinized hermaphrodites also displayed a mild tail retraction phenotype and appeared to form a male tail seam or SET cell. Surprisingly, these animals also have an exploding vulva phenotype, suggesting a possible role for seam sexual identity in vulva morphogenesis. Conversely, feminization of the male seam resulted in a significant loss of rays and the generation of ectopic alae as well as a reduced fan. Together, these data demonstrate that the sex-determination pathway functions in the seam to promote male specific neurogenesis. Using this sex-reversal strategy, we hope to identify how tra-1 regulates gene expression in the seam to promote male-specific activation of lin-32.