Fine-Tubing: Characterizing roles for Myosin II and Myosin 10A in Drosophila Tracheal Development

Abstract

Biological tubes are essential structures in organ function, facilitating the exchange of gases and nutrients. The Drosophila melanogaster trachea is a powerful model for studying tube morphogenesis, particularly terminal cells (TCs), which form elaborate seamless unicellular tubes. Although microtubule-associated motor proteins are regulators of TC morphogenesis, the role of actin-associated proteins in fine tubular networks remains less understood. Studying tube formation in the Drosophila trachea has clear clinical relevance for understanding human vascular developmental disorders. Here, we characterize necessary roles for two Myosin proteins in the proper development of the Drosophila trachea: Non-muscle Myosin II (MyoII) and Myosin 10A (Myo10A). Using a tracheal knockdown of MyoII and Myo10A activity, we discovered each protein functions to maintain the integrity of normal larval growth and the overall tracheal network. TC branching analysis across larval development showed that MyoII-depleted cells begin to exhibit reduced branch complexity, fewer branch tips, decreased path length, and reduced cell area coverage between 48 and 72 h after egg laying. These findings suggest that MyoII is especially important during this interval for branch initiation and terminal cell elaboration. Mutant TCs also supports a cell-autonomous role for MyoII activity in TC development. Perturbation of myo10A produced similar defects in terminal cell branching, tracheal morphology, and body size, suggesting that Myo10A may function similarly. Together, these findings identify MyoII and Myo10A as important regulators of the over larval body size, the Drosophila tracheal network, and seamless TCs.