Actin’ weird: why does the cell cortex contract?
Date:
Abstract: Interactions between the proteins actin and myosin govern many important cellular processes, including muscle contraction, cell motility, and cell division. Actin molecules form polarised filaments, with a barbed (or plus) and pointed (or minus) end. In actomyosin networks, myosin generates motion by binding to two actin filaments, and actively moving towards their barbed ends. In networks with random filament orientations, we might expect this to generate contraction or expansion with equal probability. However, in practice these random actomyosin networks contract, and the symmetry-breaking mechanisms that favour contraction over expansion are disputed.
We present an agent-based model for a two-dimensional random actomyosin network. Our model consists of over-damped force balance equations for actin filaments and myosin motor proteins, and incorporates cross-linking between actin filaments. At each time step, we use an energy functional minimisation method to solve for the positions of each network component and the net contractile force. Preliminary simulations suggest that the combination of cross-linking and myosin-driven motion provides a minimal mechanism for actomyosin network contraction.