Disordered actomyosin contracts in unexpected ways

The motion of living cells is in large part due to the interaction of semi-flexible actin filaments (F-actin) and myosin molecular motors, which induce the relative sliding of F-actin. It is often assumed that this simple sliding is sufficient to account for all actomyosin-based motion. While this is correct in our highly organized striated muscle, we question the application of this dogma to less ordered actomyosin systems, thus reexamining a cornerstone of our understanding of cellularmotion.