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Separate to Intercalate

PCP signaling establishes septin-mediated compartmentalization of cortical actomyosin domains to drive convergent extension during vertebrate gastrulation. Planar cell polarity (PCP) signaling establishes directionality in epithelial sheets and is important for various morphogenetic events, including convergent extension (CE) in gastrulating vertebrate embryos. During CE, mediolateral cells move toward the dorsal midline and intercalate to extend the body axis, and neural tube defects such as spina bifida result when CE is disrupted. Shindo and Wallingford investigated the link between PCP and cell shape change during intercalation of the mesoderm in gastrulating Xenopus (frog) embryos. As these approximately hexagonal cells intercalated, the anterior and posterior edges of each cell aligned roughly perpendicular to the embryonic midline, and the boundaries between the posterior face of one cell and the anterior face of a neighboring cell shortened and became enriched in phosphorylated myosin II (pMyoII). Actin accumulated at the vertices between the anteroposterior boundaries and the mediolateral sides of the cells (the mediolateral vertices), and cortical actin flowed along the anteroposterior boundaries but not along the mediolateral edges. Whereas mediolateral edges were under constant tension, the anteroposterior boundaries became increasingly taut as they shortened. Septins are GTP-binding scaffold proteins that form filaments involved in cytoskeletal dynamics, including PCP-directed cell migration and ciliogenesis. Fluorescently tagged Septin 7 (Sept7) was enriched at mediolateral vertices, and knocking down Sept7 prevented actin accumulation at these sites, blocked the tensioning of anteroposterior boundaries, increased the abundance of pMyoII, and eliminated the polar distribution of pMyoII. Knocking down the core PCP component Dishevelled interfered with the polar distribution of both Sept7 and pMyoII and decreased the abundance of pMyoII. pMyoII was required for tensioning of the anteroposterior boundaries and for normal CE. These results suggest a model in which the PCP network, which promotes the phosphorylation of MyoII, also promotes the localization of Sept7 to mediolateral vertices, thus creating separate cortical actomyosin compartments, allowing the anteroposterior actomyosin network to contract to drive intercalation. A. Shindo, J. B. Wallingford, PCP and septins compartmentalize cortical actomyosin to direct collective cell movement. Science 343, 649–652 (2014). [Abstract] [Full Text]