Rho-Kinase Directs Bazooka/Par-3 Planar Polarity during Drosophila Axis Elongation

Cell rearrangements shape the Drosophila embryo via spatially regulated changes in cell shape and adhesion. We show that Bazooka/Par-3 (Baz) is required for the planar polarized distribution of myosin II and adherens junction proteins and polarized intercalary behavior is disrupted in baz mutants. The myosin II activator Rho-kinase is asymmetrically enriched at the anterior and posterior borders of intercalating cells in a pattern complementary to Baz. Loss of Rho-kinase results in expansion of the Baz domain, and activated Rho-kinase is sufficient to exclude Baz from the cortex. The planar polarized distribution of Baz requires its C-terminal domain. Rho-kinase can phosphorylate this domain and inhibit its interaction with phosphoinositide membrane lipids, suggesting a mechanism by which Rho-kinase could regulate Baz association with the cell cortex. These results demonstrate that Rho-kinase plays an instructive role in planar polarity by targeting Baz/Par-3 and myosin II to complementary cortical domains. ► Rho-kinase is required for Baz/Par-3 planar polarity in the early Drosophila embryo ► Rho-kinase phosphorylates Baz in vitro on its C-terminal domain ► The Baz C-terminal domain is required for planar polarity in vivo ► Baz is required for polarized cell behavior during Drosophila axis elongation