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The Cytoskeletal Regulator Enabled Mediates Proper Cardiac Fusion during the Final Stages of Drosophila Dorsal Vessel Formation

Tiffany Rania King
B.S. Biology - Spelman College - 2009

Thesis Advisor: Sunita Gupta Kramer, Ph.D
Graduate Program in Cell and Developmental Biology

RWJMS, Research Tower
Room V-14

Thursday, December 11, 2014
1:00 p.m.


The Drosophila dorsal vessel (DV) is comprised of two rows of cardioblasts (CBs) that migrate toward the dorsal midline, align, and change their shape, allowing them to make dorsal and ventral attachments with their contralateral partners, in order to create a linear tube with a central lumen. A previous study in our lab has shown that DV closure occurs via a gbuttoningh mechanism where certain CBs advance ahead of their lateral neighbors, and attach creating transient holes, or small gwound-healingh like events, that will eventually seal completely by the end of development. This mechanism of sealing a hole in a developing embryo differs from that used by the overlying ectoderm, in which two epithelial sheets gzipperh from both ends to seal the embryo. In this study, we investigate the role of the actin regulator protein Enabled (Ena) in DV morphogenesis. Loss of Ena in the DV results in cell shape and alignment defects. Analysis of DV formation in ena mutants shows reduced CB leading edge protrusion length as compared to WT. Furthermore, in fixed embryos, we observe gaps in the DV between contralateral CBs. These gaps occur most often between a specific genetic subtype of CBs, which express the transcription factor seven]up and form the ostia or the valves of the heart. In WT embryos these gaps between Svp+ CBs are observed transiently during the final stages of DV closure. Taken together, our data suggest that Ena modulates the actin cytoskeleton in order to facilitate the final closing of the DV during cardiac tube formation.

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