Regulation of actin dynamics is essential during epithelial morphogenesis to allow cells to change shape, rearrange and migrate. Numerous proteins have been identified that influence actin dynamics including the Abelson (Abl) non-receptor tyrosine kinase and one of its targets Enabled (Ena). Previous work has shown that both Abl and Ena are required during epithelial morphogenesis in the embryo, including during the processes of dorsal closure and head involution. Furthermore, Abl appears to negatively regulate Ena during dorsal closure by reducing the levels of Ena available to assist with the formation of filopodia by the leading edge epithelial cells. To identify additional proteins that may function with Abl and/or Ena during epithelial morphogenesis, we are collaborating with Traci Stevens’ lab at Randolph-Macon College. The Stevens lab has carried out a genetic screen to identify mutations in genes that dominantly enhance or suppress the epithelial defects caused by overexpressing a constitutively active form of Abl called BCR-Abl. One of the genes they identified is gartenzwerg (garz), an ARF-GEF. We have found that mutations in garz dominantly enhance the head involution phenotype of ena homozygous mutants, but appear to have essentially no effect on the dorsal closure phenotype of these mutants. Interestingly, examination of the levels and localization of Ena and actin in garz mutant embryos has not yet revealed head involution defects, but has revealed dorsal closure defects that are consistent with a potential role for Garz in regulating contraction of the leading edge actin/myosin cable. To examine whether Garz may be functioning as a canonical ARF-GEF during epithelial morphogenesis we are currently testing whether mutations in ArfGAP1 or Arf79F also dominantly modify the ena homozygous mutant phenotype. The continued examination of the roles of these proteins during dorsal closure may reveal novel roles for the Arf family of small GTPases during epithelial morphogenesis.