Cardiogenesis is a complex process that requires a series of specifically synchronized cellular events leading to the formation of a heart tube. Cardioblasts (CBs) must migrate towards the midline of the developing embryo and undergo cell shape changes to facilitate lumen formation. Rac1 has previously been shown to mediate cell movement, shape, and adhesion through the actin cytoskeleton. However, the role of Rac1 in dorsal vessel (DV) formation remains unclear. Here, we expressed Rac1 gain-of-function (GOF) and loss-of-function (LOF) mutants specifically in the Drosophila DV and examined embryos for cardiac abnormalities. When constitutively active Rac1 was expressed in the entire DV, we observed misalignment of CBs, gaps between CB pairs, and overall abnormal morphology of the CBs. Restricted overexpression of constitutively active Rac1 to a subset of CBs caused CB clusters and misalignments. These findings suggest that proper regulation of Rac1 signaling activity is required in all CBs for proper DV formation.
***Please italicize the wordDrosophila in the title. Thanks.
