Event

Abstract: Many essential cellular processes depend on subcellular structures capable of generating active forces. In particular, actomyosin networks and their contraction are central for cell organization, shape, and motility. However, the relative importance of active local stresses, network deformation, external friction, and geometry is still not well understood. In vitro experiments with reconstituted actomyosin networks on micropatterned surfaces have shown a robust contraction bias to higher friction surfaces, while an remarkable insensitivity to the distribution of myosin motors driving the dynamics. In this talk, I will review the experimental results, and present a mathematical model of the actomyosin network as a 2D deformable viscoelastic cable-network material with active contractile stresses. I will then demonstrate how, through analysis and simulation, our model reproduces key experimental results. Notably, I will explain why friction, not myosin, determines the contractile trajectories, shedding light on the importance of mechanical effects over biochemical ones. This work demonstrates how homogeneous networks could contract asymmetrically in cells and tissues, and has broad implications of how contractile actin networks might behave in cells which can generate or harness gradients of resistive forces.