摘要：SummaryCell shape changes from locomotion to cytokinesis are, to a large extent, driven by myosin-driven remodeling of cortical actin patterns. Passive crosslinkers such as α-actinin and fascin as well as actin nucleator Arp2/3 complex largely determine actin network architecture and, consequently, membrane shape changes. Here we reconstitute actomyosin networks inside cell-sized lipid bilayer vesicles and show that depending on vesicle size and concentrations of α-actinin and fascin actomyosin networks assemble into ring and aster-like patterns. Anchoring actin to the membrane does not change actin network architecture yet exerts forces and deforms the membrane when assembled in the form of a contractile ring. In the presence of α-actinin and fascin, an Arp2/3 complex-mediated actomyosin cortex is shown to assemble a ring-like pattern at the equatorial cortex followed by myosin-driven clustering and consequently blebbing. An active gel theory unifies a model for the observed membrane shape changes induced by the contractile cortex.Graphical abstractDisplay OmittedHighlights•Myosin, α-actinin, and fascin drive the formation of diverse actin patterns in GUVs•A self-assembling membrane-bound contractile ring pattern slightly deforms GUVs•Dendritic actomyosin requires actin crosslinkers for clustering and GUV blebbing•A physical model describes membrane deformation at the site of actomyosin clusterMechanobiology; Biological sciences; Cell biology
