Abelson kinase modulates epithelial morphogenesis. E.E. Grevengoed , T. Jesse , J. Loureiro , M. Peifer. Dept Biol, Univ North Carolina, Chapel Hill, NC.

   Adherens junctions (AJs) mediate many processes necessary to maintain epithelial integrity. During morphogenesis, epithelial cells reorganize and change shape, requiring modulation of adhesion at AJs. We have identified a role for the non-receptor tyrosine kinase Abelson (Abl) during epithelial development, potentially acting to modulate AJ function during morphogenesis. Maternal and zygotic abl mutants exhibit defects in germ band retraction, dorsal closure and head involution, three processes that require cell shape changes. Analysis of dorsal closure shows that cells fail to uniformly change shape during this process. These mutants also have an altered localization of Actin and Enabled (Ena), an Abl substrate involved in modulating actin dynamics, at the leading edge of the dorsal closure front. Mutations in ena suppress the abl morphogenesis defects, suggesting it may be an Abl target in this process. Ena co-localizes with Armadillo (Arm) at AJs throughout most stages of epithelial development and mutations in ena enhance arm dorsal closure defects. Consistent with this, mutations in shotgun (DE- Cadherin) enhance the defects found in abl mutants. Finally, Arm and a-catenin levels in AJs are reduced in the abl mutants. These data suggest a role for Abl signaling during epithelial development. Surprisingly, we have also found a role for Abl during syncytial development. abl mutants show actin cytoskeletal defects during both nuclear divisions 10-13 as well as cellularization. AJ proteins co-localize with Actin at pseudocleavage furrows and also localize to the invaginating cellularization furrow. One hypothesis we are testing is that Abl signaling effects AJ protein localization and this in turn disrupts cytoskeletal dynamics.