Contractility regulation in the cortex, flows, and symmetry breaking. (A). Mechanochemical feedback in a simplified one dimensional actomyosin cortex. A localized increase in bound myosin concentration (green) creates higher contractile stress than elsewhere. The resulting force advects myosin, tending to reinforce the initial increase, which is counteracted by diffusion. Co-advection of actin (gray) has an inhibitory effect, because of opposing compressive stress and turnover, which penalizes density changes away from the initial, homeostatic state. In the inhomogeneous patterned state, steady-state state flows, in the presence of a momentum absorbing substrate, can give rise to migration. (B) Proposed migration mechanism based on theory of self-organized active tube patterning Mietke et al. (2019b). A contractility-based instability on the tube surface leads to an inhomogeneous active stress regulator profile, as in panel (A). This concentrates the active stress and pinches the tube. A situation where the regulator peak is centered on the pinch (Stationary) may be unstable (see text), giving rise to a broken symmetry state. This state is characterized by peristaltic surface waves; in the presence of an outer fluid, directed motion would occur.