Talin is required to position and expand the luminal domain of the Drosophila heart tube

• Talin is an early marker of the Drosophila heart lumen initiation site.
• Talin is required for heart cell migratory dynamics, polarity, and lumen formation.
• In mutant embryos, Robo and Dystroglycan enriched mini-lumens develop ectopically.
• A Talin transgene lacking actin binding is unable to enlarge the heart lumen.

Fluid- and gas-transporting tubular organs are critical to metazoan development and homeostasis. Tubulogenesis involves cell polarization and morphogenesis to specify the luminal, adhesive, and basal cell domains and to establish an open lumen. We explore a requirement for Talin, a cytoplasmic integrin adapter, during Drosophila melanogaster embryonic heart tube development. Talin marks the presumptive luminal domain and is required to orient and develop an open luminal space within the heart. Genetic analysis demonstrates that loss of zygotic or maternal-and-zygotic Talin disrupts heart cell migratory dynamics, morphogenesis, and polarity. Talin is essential for subsequent polarization of luminal determinants Slit, Robo, and Dystroglycan as well as stabilization of extracellular and intracellular integrin adhesion factors. In the absence of Talin function, mini-lumens enriched in luminal factors form in ectopic locations. Rescue experiments performed with mutant Talin transgenes suggest that actin-binding is required for normal lumen formation, but not for initial heart cell polarization. We propose that Talin provides instructive cues to position the luminal domain and coordinate the actin cytoskeleton during Drosophila heart lumen development.