F-actin buckling coordinates contractility and severing in a biomimetic actomyosin cortex

摘要: Here we develop a minimal model of the cell actomyosin cortex by forming quasi-2D cross-linked filamentous actin (F-actin) network adhered to membrane and contracted myosin thick filaments. Myosin motors generate both compressive tensile stresses on F-actin consequently induce large bending fluctuations, which reduces their effective persistence length <1 μm. Over range conditions, show extent contraction corresponds exactly individual shortening via buckling. This demonstrates an essential role buckling in breaking symmetry between facilitate mesoscale up 80% strain. Portions buckled with radius curvature ~300 nm are prone severing thus mechanically coordinate contractility severing, initial step turnover. Finally, acquired myosin-induced can be further constrained adhesion membrane, accelerating filament but inhibiting long-range transmission necessary for contractility. Thus, regulate coupling severing. These data demonstrate nonlinear response potentiating myosin-mediated may serve as general mechanism cortical dynamics across diverse assemblies smooth muscle nonmuscle cells.