Active mechanics of starfish oocytes

Actomyosin is a canonical example of an active material, driven out of equilibrium in part through the injection of energy by myosin motors. This influx of energy allows actomyosin networks to generate cellular-scale contractility, which underlies cellular processes ranging from division to migration. While the molecular players underlying actomyosin contractility have been well characterized, how cellular-scale deformation in disordered actomyosin networks emerges from filament-scale interactions is not well understood. Here, we address this question in vivo using the meiotic surface contraction wave of starfish oocytes. Using pharmacological treatments targeting actin polymerization, we find that the rate of cellular deformation is not a monotonic function of cortical actin density, but is instead peaked near the wild type density. To understand this, we develop an active fluid model coarse-grained from filament-scale interactions and find quantitative agreement with the measured data. This model further predicts the dependence of the strain rate on the concentrations of active motors and passive actin crosslinkers, which we experimentally verify. Taken together, this work is an important step towards bridging the molecular and cellular length scales for cytoskeletal networks.