Abstract
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.