Affiliation: College of Arts and Sciences, Department of Biology
Without proper apicobasal polarity, epithelial cells cannot properly assemble into various tissues or change cell shape in a coordinated fashion to allow for proper development. Loss of polarity in Drosophila embryonic development leads to defects in cell-cell adhesion as adhesion complexes are no longer proper localized, disrupting coordination of the actin cytoskeletons between the cells that make up a tissue. As a result, tissues quickly become disorganized, appearing multilayered. Here, we show that loss of the small GTPase Rap1 causes defects in apical constriction during Drosophila gastrulation, leading to a failure to properly invaginate the mesoderm. This suggested that Rap1 modulates connection of adherens junctions to the actin cytoskeleton. As a result, we broadened our initial studies to learn the role of Rap1 in regulating the actin cytoskeleton and polarity during morphogenesis. In embryos lacking maternal and zygotic Rap1, we observed early defects in the localization of the apical polarity proteins, Baz and aPKC. Additionally, Rap1 mutants exhibit defects in apical tension as the sizes of cell apices in mutants wildly vary from cell to cell. Further exploration of these initial results suggests that Rap1 performs a critical role in the regulation of the establishment and elaboration of apical polarity during early Drosophila embryogenesis.