Characterization of Enabled function during epithelial morphogenesis. J. Gates ¹, E.E. Grevengoed ², T.L. Jesse ¹, M. Peifer ^1,2. 1) Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC; 2) Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC.

   Intercellular adhesion and the actin cytoskeleton must be regulated during development to accommodate changes in cell shape, cell rearrangements and cell migrations that occur as the embryo is shaped. If they are not properly regulated, morphogenetic processes such as dorsal closure and head involution are disrupted. Dorsal closure and head involution defects are observed in animals carrying mutations in genes encoding integral components of the adherens junction, DE-cadherin and Armadillo (Arm). Similar defects are seen in animals maternally and zygotically mutant for the nonreceptor tyrosine kinase Abelson (Abl). Enabled (Ena) is a substrate of Abl. We have found that ena genetically interacts with abl and arm in the epidermis and colocalizes with Arm at the adherens junction. Recently, mammalian Ena/VASP proteins have been shown to promote cell adhesion and limit cell motility by regulating localized actin polymerization. This raises the possibility that Ena functions at the adherens junction during epithelial morphogenesis to regulate adhesion by regulating actin polymerization. The results of our efforts to investigate this possibility will be presented.