Polarized contraction coupled to F-actin turnover is required for pulsed contractions. Adam C. Martin, Frank M. Mason, Mike Tworoger. Biology, Massachusetts Institute of Technology, Cambridge, MA.

   Apical constriction of epithelial cells promotes tissue folding during developmental processes such as gastrulation. Apical constriction and mesoderm invagination of the Drosophila ventral furrow is facilitated by pulsed contractions of an actin filament (F-actin) and myosin-II network that spans the apical surface and is coupled to circumferential adherens junctions. The mechanisms that generate pulsed actin-myosin contractions at the middle of the apical surface (medial cortex) are not known. Here, we combine live imaging, quantitative image analysis, spatially controlled drug injections, and genetics to demonstrate that F-actin turnover (assembly and disassembly) is critical for pulsed contractions. Apical constriction requires F-actin disassembly/remodeling after contraction pulses to prevent medial F-actin accumulation in ventral furrow cells. F-actin assembly, at least partially mediated by the formin Diaphanous, maintains a continuous medial actin-myosin meshwork, which is critical for contraction pulses and cell-cell adhesion. We show that actin-myosin contraction is directed towards medial Rho Kinase (Rok) foci and requires Rok activity. We propose that Rok and possibly other signals establish a radial planar cell polarity in ventral furrow cells that result in cycles of medial-directed contraction followed by actin-myosin network turnover to generate contractile pulses.