Apical domain polarization localizes actin–myosin activity to drive ratchet-like apical constriction

Abstract

Apical constriction promotes epithelia folding, which changes tissue architecture. During Drosophila gastrulation, mesoderm cells exhibit repeated contractile pulses that are stabilized such that cells apically constrict like a ratchet. The transcription factor Twist is required to stabilize cell shape, however it is unknown how Twist spatially coordinates downstream signals to prevent cell relaxation. We find that during constriction, Rho-associated kinase (Rok) is polarized to the middle of the apical domain (medioapical cortex), separate from adherens junctions (AJs). Rok recruits or stabilizes medioapical myosin II (Myo-II), which contracts dynamic medioapical actin cables. The formin Diaphanous mediates apical actin assembly to suppress medioapical E-Cadherin localization and form stable connections between the medioapical contractile network and AJs. Twist is not required for apical Rok recruitment, but instead polarizes Rok medioapically. Therefore, Twist establishes “radial” cell polarity of Rok/Myo-II and E-Cadherin and promotes medioapical actin assembly in mesoderm cells to stabilize cell shape fluctuations.

Coronin 1B supports RhoA signaling at cell-cell junctions through Myosin II

“…7 RhoA signaling is a master regulator of actomyosin cytoskeleton and thus has been implicated in a variety of morphogenetic processes. [31][32][33][34][35][36] While the role for active RhoA signaling in facilitating essential cellular processes has been wellestablished 9,[37][38][39][40][41] there are circumstances where RhoA signaling must be downregulated, either physiologically or pathologically to elicit a biological response. 41,42 Given the importance of the actomyosin cytoskeleton in positively regulating RhoA signaling, 7,[43][44][45] targeting actin-regulators such as Coronin 1B might be one of the approaches to achieve a precise spatiotemporal regulation of RhoA.…”

Apical constriction is driven by a pulsatile apical myosin network in delaminating Drosophila neuroblasts

“…The formation of medial myosin pulses is dependent on a radialpolarized actin network with the pointed ends of actin filaments enriched in the medioapical region of ventral furrow cells (Coravos and Martin, 2016;Mason et al, 2013;Vasquez et al, 2014). Lowdose cytochalasin D (CytoD) treatment is a widely used method to disrupt the radial polarized apical actin network, and to block medial myosin pulses in ventral furrow cells (Coravos and Martin, 2016;Mason et al, 2013) and in cells undergoing shape deformation during Drosophila germband extension (Munjal et al, 2015).…”

“…Lowdose cytochalasin D (CytoD) treatment is a widely used method to disrupt the radial polarized apical actin network, and to block medial myosin pulses in ventral furrow cells (Coravos and Martin, 2016;Mason et al, 2013) and in cells undergoing shape deformation during Drosophila germband extension (Munjal et al, 2015).…”

“…For example, in ventral furrow cells undergoing invagination as a group of cells in Drosophila embryos the myosin foci and fibers arise across the apical surface, move to the center of the cells, form large spots with high intensity and disperse. This nonjunctional myosin movement on the cell apical surface was termed medial myosin pulses, and each pulse coincides with a rapid apical area constriction phase (Martin et al, 2009;Mason et al, 2013). The amnioserosa cells also assemble a dynamic medial actomyosin network that drives apical cell shape fluctuations during the Drosophila dorsal closure process (Blanchard et al, 2010;David et al, 2010).…”

Myosin II is not required for Drosophila tracheal branch elongation and cell intercalation

“…1C,D). Furthermore, it has been suggested previously that a loss of MyoII function results in cortical relaxation (Mason et al, 2013;Royou et al, 2002;Rozbicki et al, 2015). We therefore investigated whether knockdown of Sqh-GFP resulted in aberrant cell morphology.…”