Simulating contraction of disordered actomyosin networks
Date:
Abstract: The mechanics of actin and myosin in the cell cortex govern important cellular processes, including division, shape change, and motility. Actin molecules form polarised filaments (with a plus and minus end), and myosin generates motion by binding to two actin filaments, and moving actively towards their plus ends. Experiments have shown that myosin generates contraction in networks with filaments initially distributed at random. However, the microscopic mechanisms that cause this contraction remain unknown.
We develop a two-dimensional agent-based model for disordered actomyosin networks. Using repeated simulations, we show that protein friction (arising from cross-linking or filament contact) can induce contraction of semi-flexible filaments. We then use these simulations to explore how cytoplasm viscosity, filament turnover, and the dynamics of a single dipole influence contractility.