We use mathematical modelling and computation to investigate how protein friction facilitates contraction of disordered actomyosin networks. We simulate two-dimensional networks using an agent-based model, consisting of a system of force-balance equations for myosin motor proteins and semi-flexible actin filaments. A major advantage of our approach is that it enables direct calculation of the network stress tensor, which provides a quantitative measure of contractility. Exploiting this, we use repeated simulations of disordered networks to confirm that both protein friction and actin filament bending are required for contraction. We then use simulations of elementary two-filament assemblies to show that filament bending flexibility can generate contraction on the microscopic scale. Finally, we show that actin filament turnover is necessary to sustain contraction and prevent pattern formation. Simulations with and without turnover also exhibit contractile pulses. However, these pulses are aperiodic, suggesting that periodic pulsation can only be achieved by additional regulatory mechanisms.

中文翻译：

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蛋白质摩擦和细丝弯曲促进收缩性放线菌素网络的收缩

我们使用数学建模和计算来研究蛋白质摩擦如何促进无序放线菌素网络的收缩。我们使用基于代理的模型模拟二维网络，该模型由肌球蛋白运动蛋白和半柔性肌动蛋白丝的力平衡方程组组成。我们方法的主要优点是，它可以直接计算网络应力张量，从而提供定量的收缩率度量。利用这一点，我们使用无序网络的重复模拟来确认蛋白质摩擦和肌动蛋白丝弯曲都需要收缩。然后，我们使用基本的两丝组件的模拟来显示，丝弯曲的柔性可以在微观尺度上产生收缩。最后，我们表明肌动蛋白丝周转是维持收缩和防止模式形成所必需的。有或没有翻转的模拟也显示出收缩脉冲。但是，这些脉冲是非周期性的，这表明只能通过其他调节机制才能实现周期性的脉动。