Abstract
We report cloning and characterization of coro, which codes for the Drosophila homologue of the F-actin binding protein coronin. Viable alleles of coro produce a variety of phenotypes in leg, wing and eye development, which are similar to the phenotypes observed as a result of mutations in genes associated with the actin cytoskeleton and/or membrane trafficking. Homozygous lethal mutations in coro results in the disruption of the actin cytoskeleton in wing imaginal discs. Formation of both basolateral septate junctions and apical adherens junctions are also adversely affected in epithelial cells. Both viable and lethal alleles of coro show genetic interactions with syntaxin1A, a gene required for membrane trafficking. They also show enhanced response to over-expression of Decapentaplegic (Dpp) and its receptor Thick vein. Tracing of Dpp morphogen using a Dpp::GFP fusion construct suggested defects in the endocytic pathway, which resulted in uniform distribution of Dpp along the AP axis rather than a gradient from the AP boundary. Our results provide a genetic link between endocytosis/exocytosis events involving F actin-coated vesicles and the establishment of morphogen gradient.
