Department of Biomedical Engineering, Yale University, 55 Prospect Street, New Haven, Connecticut 06520, USA.
Systems Biology Institute, Yale University, 850 West Campus Drive, West Haven, Connecticut 06516, USA.
Nat Commun. 2016 Aug 25;7:12615. doi: 10.1038/ncomms12615.
While the molecular interactions between individual myosin motors and F-actin are well established, the relationship between F-actin organization and actomyosin forces remains poorly understood. Here we explore the accumulation of myosin-induced stresses within a two-dimensional biomimetic model of the disordered actomyosin cytoskeleton, where myosin activity is controlled spatiotemporally using light. By controlling the geometry and the duration of myosin activation, we show that contraction of disordered actin networks is highly cooperative, telescopic with the activation size, and capable of generating non-uniform patterns of mechanical stress. We quantitatively reproduce these collective biomimetic properties using an isotropic active gel model of the actomyosin cytoskeleton, and explore the physical origins of telescopic contractility in disordered networks using agent-based simulations.
虽然单个肌球蛋白分子与 F-肌动蛋白之间的分子相互作用已经得到很好的确立，但 F-肌动蛋白的组织与肌球蛋白力之间的关系仍未被很好地理解。在这里，我们探索了肌球蛋白诱导的应力在二维生物仿生无序肌动球蛋白细胞骨架模型中的积累，其中肌球蛋白活性是使用光进行时空控制的。通过控制肌球蛋白激活的几何形状和持续时间，我们表明无序肌动蛋白网络的收缩具有高度的协同性，与激活大小成比例，并且能够产生非均匀的机械应力模式。我们使用肌动球蛋白细胞骨架的各向同性活性凝胶模型定量再现了这些集体仿生特性，并使用基于代理的模拟探索了无序网络中伸缩收缩的物理起源。
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