Drosophila Integrins Act in Conjunction with Robo to Establish Heart Cell Polarity

Abstract

<p>The Drosophila heart arises from the migration and subsequent fusion of bilateral rows of cardioblasts into a single dorsal vessel at the midline. Previous studies have demonstrated that the coordinated migration, and formation of a lumen in the Drosophila heart requires signalling by Slit, which is secreted by the cardioblasts and binds to Robo receptors on the same cells. Cardioblasts also express a single Integrin dimer, αPS3/βPS1, and as key factors in cell migration and cell-matrix adhesion, are required for assembly of the heart. Embryos heterozygous for a null allele of slit or scab have normal heart development however when gene dosage in the Slit and Integrin pathways are altered simultaneously more than additive effects such as delayed migration of cardial cells, cell clumping and midline crossing, suggest that the two pathways intersect upon a common function. This thesis demonstrates that reduced Integrin function delays the acquisition of cell polarity by heart cells and prevents lumen formation. Furthermore, localization of Robo to the heart lumen requires Integrin function , and reciprocally, Robo function is required for proper Integrin distribution. These findings support a role for Integrins working in conjunction with Robo in the establishment of heart cell polarity and revealed the complexity of this interaction.</p>