Role of Myosin II and its regulators in cortical cap remodeling in the syncytial Drosophila embryo

Abstract

Cell shape change is crucial to many biological processes such as cell migration and cytokinesis. The cortical actin cytoskeleton controls cell shape remodeling. Drosophila embryogenesis offers a suitable model to study protrusive and deformative forces exerted by cortical actin networks. The early Drosophila embryo develops as a syncytium during the first 13 synchronized nuclear divisions. Divisions 10-13 take place in the cortex. Between each nucleus and the plasma membrane is a cortical actin ‘cap’ bearing numerous apical F-actin protrusions called microvilli. Caps expand from interphase to metaphase of each cycle 10-13, accompanied by a decrease in the lengths of their microvilli. Myosin II has been implicated in the regulation of cap expansion dynamics and is therefore a candidate for the regulation of microvillar remodeling. To test this, we perturbed Myosin II by knocking down or overexpressing various players in the Rho pathway. We found that Myosin II contractility is required for the appropriate morphology and architecture of the microvilli. We also explored a role for another downstream effector of Rho, the formin Diaphanous, in regulating microvilli and found that Diaphanous is necessary to form microvilli in a manner independent of the Rho pathway. Our results show that Myosin II and Diaphanous regulate the formation of microvilli by different mechanisms. Our work demonstrates a hitherto unknown role for Myosin II contractility in forming and stabilizing actin protrusions.