Actomyosin networks play essential roles in many cellular processes including intracellular transport, cell division, and cell motility, exhibiting a myriad of spatiotemporal patterns. Despite extensive research, how the interplay between network mechanics, turnover and geometry leads to these different patterns is not well understood. We focus on the size-dependent behavior of contracting actomyosin networks in the presence of turnover, using a reconstituted system based on cell extracts encapsulated in water-in-oil droplets. We find that the system can self-organize into different global contraction patterns, exhibiting persistent contractile flows in smaller droplets and periodic contractions in the form of waves or spirals in larger droplets. The transition between continuous and periodic contraction occurs at a characteristic length scale that is inversely dependent on the network contraction rate. These dynamics are recapitulated by a theoretical model, which considers the coexistence of different local density-dependent mechanical states with distinct rheological properties. The model shows how large-scale contractile behaviors emerge from the interplay between network percolation essential for long-range force transmission and rearrangements due to advection and turnover. Our findings thus demonstrate how varied contraction patterns can arise from the same microscopic constituents, without invoking specific biochemical regulation, merely by changing the system′s geometry.

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The shape of cells is the outcome of the balance of inner forces produced by the acto-myosin network and the resistive forces produced by cell adhesion to their environment. The specific contributions of contractile, anchoring and friction forces to network deformation rate and orientation are difficult to disentangle in living cells where they influence each other. Here, we reconstituted contractile acto-myosin networks in vitro to study specifically the role of the friction forces between the network and its anchoring substrate. To modulate the magnitude and spatial distribution of friction forces, we micropatterned actin nucleation promoting factors on glass or on a lipid bilayer. We adapted their concentrations on each surface to induce the assembly of actin networks of similar densities, and compare the deformation of the network toward the centroid of the pattern shape upon myosin-induced contraction. We found that actin network deformation was faster and more coordinated on lipid bilayers than on glass, showing the resistance of friction to network contraction. To further study the role of the spatial distribution of these friction forces, we designed heterogeneous micropatterns made of glass and lipids. The deformation upon contraction was no longer symmetric but biased toward the region of higher friction. Furthermore, we showed that the pattern of friction could robustly drive network contraction and dominate the contribution of asymmetric distributions of myosins. Therefore, we demonstrate that during contraction both the active and resistive forces are essential to direct the actin network deformation.