Rac is a Rho family GTPase that controls actin cytoskeletal dynamics and cell migration and is a major target of Ras during oncogenic transformation. We are using vulval development as a model system to study Rac function as it involves several different processes potentially influenced by Rac, including Ras-MAP kinase signaling, cell proliferation and cell migration. We had previously reported that two rac genes, mig-2 and ced-10 , function redundantly during vulval morphogenesis, that mig-2(gf) alleles have dominant negative characteristics and that UNC-73 seems to be the major GEF for MIG-2 and CED-10 in this process . In either mig-2(gf ), mig-2(lf);ced-10(RNAi) or unc-73(lf) mutants, P5.p and/or P7.p descendants failed to join the central invagination (migration defect) and in a low percentage of the animals , failed to adopt vulval fates. Further, Nomarski analysis of the final vulval-specific division in mig-2(gf) animals showed a change of the ‘T’ polarity of the secondary vulval cell descendants to ‘L’ or ‘O’ so that these cells show NLLL or NOLL polarity instead of the wild-type NTLL. Cells exhibiting this changed polarity also showed a migration defect indicating that the two phenotypes may be related. Vulval development thus offers a good system to identify and distinguish between the different rac-associated phenotypes. Alleles of mig-15 , a worm ortholog of Drosophila misshapen and a ste-20 family member (1) showed similar phenotypes. Based on the similarity of phenotypes and the molecular nature of these genes, mig-2 and ced-10 may act in the same or in a parallel pathway with mig-15 to control migration of P5.p and P7.p descendants and additionally may interact with genes that specify the secondary fate. We have generated transgenic animals expressing the activating ( mig-2 G16R), dominant negative ( mig-2 T21N) and WT mig-2 constructs under the lin-31 promoter to circumvent the pleiotropies associated with the mig-2 alleles. This experiment also showed that expression of these constructs in the vulva mimicked the vulval phenotypes of mig-2(gf) and mig-2(lf);ced-10 (RNAi) mutants. We are currently using these transgenics to test the interaction of mig-2 with unc-73 and mig-15 as well as with genes known to be involved in patterning of secondary vulval cells. (1) Zhu, X., and Hedgecock, E., WBG 14(5): 76, 1997.