Mechanical forces play a crucial role in diverse physiological processes, such as cell migration, cytokinesis, and morphogenesis. The actin cytoskeleton generates a large fraction of the mechanical forces via molecular interactions between actin filaments (F‐actins) and myosin motors. Recent studies have shown that the common tendency of actomyosin networks to contract into a smaller structure deeply involves F‐actin buckling induced by motor activities, fragmentation of F‐actins, and the force‐dependent unbinding of cross‐linkers that inter‐connect F‐actins. The fragmentation of F‐actins was shown to originate from either buckling or tensile force from previous single‐molecule experiments. While the role of buckling in network contraction has been studied extensively, to date, the role of tension‐induced F‐actin fragmentation in network contraction has not been investigated. In this study, we employed in vitro experiments and an agent‐based computational model to illuminate when and how the tension‐induced F‐actin fragmentation facilitates network contraction. Our experiments demonstrated that F‐actins can be fragmented due to tensile forces, immediately followed by catastrophic rupture and contraction of networks. Using the agent‐based model, we showed that F‐actin fragmentation by tension results in distinct rupture dynamics different from that observed in networks only with cross‐linker unbinding. Moreover, we found that tension‐induced F‐actin fragmentation is particularly important for the contraction of networks with high connectivity. Results from our study shed light on an important regulator of the contraction of actomyosin networks which has been neglected. In addition, our results provide insights into the rupture mechanisms of polymeric network structures and bio‐inspired materials.

中文翻译：

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肌球蛋白诱导的 F-肌动蛋白断裂促进肌动蛋白网络的收缩

机械力在细胞迁移、胞质分裂和形态发生等多种生理过程中发挥着至关重要的作用。肌动蛋白细胞骨架通过肌动蛋白丝（F-肌动蛋白）和肌球蛋白马达之间的分子相互作用产生大部分机械力。最近的研究表明，肌动球蛋白网络收缩成更小的结构的共同趋势深深地涉及运动活动引起的 F-肌动蛋白屈曲、F-肌动蛋白的断裂以及将 F-肌动蛋白相互连接的交联剂的力依赖解结合。肌动蛋白。先前的单分子实验表明，F-肌动蛋白的断裂源自屈曲力或张力。虽然屈曲在网络收缩中的作用已被广泛研究，但迄今为止，张力诱导的 F-肌动蛋白断裂在网络收缩中的作用尚未得到研究。在这项研究中，我们采用体外实验和基于代理的计算模型来阐明张力诱导的 F-肌动蛋白断裂何时以及如何促进网络收缩。我们的实验表明，F-肌动蛋白可能会因拉力而断裂，紧接着网络会发生灾难性的破裂和收缩。使用基于代理的模型，我们表明，张力导致的 F-肌动蛋白断裂会导致明显的断裂动力学，这与仅在交联剂解离的网络中观察到的情况不同。此外，我们发现张力诱导的 F-肌动蛋白断裂对于高连通性网络的收缩特别重要。我们的研究结果揭示了一直被忽视的肌动球蛋白网络收缩的重要调节因子。此外，我们的结果还为聚合物网络结构和仿生材料的破裂机制提供了见解。