PCP and Septins Compartmentalize Cortical Actomyosin to Direct Collective Cell Movement

Sculpting Actomyosin The sculpting of embryos during development involves coordinated movement of cells in large groups. How actomyosin is controlled during such collective cell movement remains poorly understood. Working with developing Xenopus mesoderm, Shindo and Wallingford (p. 649) found that planar cell polarity proteins and septins interface with the actomyosin machinery to control collective cell movement. A mechanism is revealed for orchestrated cell movement during gastrulation in Xenopus. Despite our understanding of actomyosin function in individual migrating cells, we know little about the mechanisms by which actomyosin drives collective cell movement in vertebrate embryos. The collective movements of convergent extension drive both global reorganization of the early embryo and local remodeling during organogenesis. We report here that planar cell polarity (PCP) proteins control convergent extension by exploiting an evolutionarily ancient function of the septin cytoskeleton. By directing septin-mediated compartmentalization of cortical actomyosin, PCP proteins coordinate the specific shortening of mesenchymal cell-cell contacts, which in turn powers cell interdigitation. These data illuminate the interface between developmental signaling systems and the fundamental machinery of cell behavior and should provide insights into the etiology of human birth defects, such as spina bifida and congenital kidney cysts.