Department of Physics, Center for Theoretical Biological Physics, University of California at San Diego, La Jolla, CA 92093, USA.
Proc Natl Acad Sci U S A. 2012 Apr 24;109(17):6446-51. doi: 10.1073/pnas.1204205109. Epub 2012 Apr 9.
Contractile forces are essential for many developmental processes involving cell shape change and tissue deformation. Recent experiments on reconstituted actomyosin networks, the major component of the contractile machinery, have shown that active contractility occurs above a threshold motor concentration and within a window of cross-link concentration. We present a microscopic dynamic model that incorporates two essential aspects of actomyosin self-organization: the asymmetric load response of individual actin filaments and the correlated motor-driven events mimicking myosin-induced filament sliding. Using computer simulations, we examine how the concentration and susceptibility of motors contribute to their collective behavior and interplay with the network connectivity to regulate macroscopic contractility. Our model is shown to capture the formation and dynamics of contractile structures and agree with the observed dependence of active contractility on microscopic parameters, including the contractility onset. Cooperative action of load-resisting motors in a force-percolating structure integrates local contraction/buckling events into a global contractile state via an active coarsening process, in contrast to the flow transition driven by uncorrelated kicks of susceptible motors.
收缩力对于涉及细胞形状变化和组织变形的许多发育过程至关重要。最近在重组成肌动球蛋白网络（收缩机械的主要成分）的实验中表明，活跃的收缩力发生在一个临界的马达浓度之上，并在交联浓度的窗口内。我们提出了一个微观动态模型，该模型包含了肌动球蛋白自组织的两个基本方面：单个肌动蛋白丝的不对称负载响应，以及模拟肌球蛋白诱导丝滑动的相关马达驱动事件。通过计算机模拟，我们研究了马达的浓度和敏感性如何有助于它们的集体行为，并与网络连接相互作用来调节宏观收缩性。我们的模型被证明可以捕捉收缩结构的形成和动力学，并与观察到的主动收缩性对微观参数的依赖性一致，包括收缩性开始。在力渗透结构中抵抗负载的马达的协同作用通过主动粗化过程将局部收缩/弯曲事件整合到全局收缩状态中，与由易感性马达的不相关踢动驱动的流动转变形成对比。
