Model for mechanism and function of contractile pulses. (A) Myo-II dynamics during a contractile pulse. The contractile pulse is initiated by a local increase in Rok activity that elevates Myo-II phosphorylation and activity. Myo-II coalescence into medioapical foci results from cortical flow (red arrows) resulting from a gradient in cortical tension and net Myo-II minifilament assembly (dark green) at Rok foci with net minifilament disassembly (light blue) in regions of low Rok by myosin phosphatase (purple). Decreased Rok activity after Myo-II coalescence results in Myo-II dephosphorylation followed by remodeling of the contracted cortex. (B) Contractile pulses are required to maintain tissue integrity. Pulsatile Myo-II contraction occurs asynchronously in adjacent cells, which reduces stress at adherens junctions. In addition, Myo-II remodeling allows cells to adjust contacts to maintain stable intercellular cytoskeletal connections. Continuous Myo-II assembly and apical constriction decreases ability of actomyosin networks to dynamically adjust to changes in tissue mechanics, resulting in stretching of Myo-II structures and loss of intercellular connections (red arrows).