论文标题
解构肌球蛋白收缩性在焦点粘附中的力波动中的作用
Deconstructing the role of myosin contractility in force fluctuations within focal adhesions
论文作者
论文摘要
将细胞连接到其细胞外环境的局灶性粘连（FAS）中表现出的力波动，表明控制细胞迁移的基础机械的复杂作用。为了阐明肌球蛋白电动机在时间牵引力振荡中的明确作用，我们根据分子离合器假设的动力学模型改变了这些电动机的收缩力。随着收缩力的降低，通过改变运动速度和依恋/脱离速率来实现，我们在实验相关的参数空间中进行了分析表明，系统从衰减的振荡到稳定的极限周期振荡，通过超临界型HOPF分叉。作为运动活动和离合器数量的函数，系统表现出各种动力学状态。我们通过运动离合器系统的随机模拟来证实我们的分析结果。如我们的模型所预测的，我们在参数状态下获得了极限周期振荡。平均离合器和运动变形中振荡的频率范围与实验结果很好地比较。
Force fluctuations exhibited in focal adhesions (FAs) that connect a cell to its extracellular environment, point to the complex role of the underlying machinery that controls cell migration. To elucidate the explicit role of myosin motors in the temporal traction force oscillations, we vary the contractility of these motors in a dynamical model based on the molecular clutch hypothesis. As the contractility is lowered, effected both by changing the motor velocity and the rate of attachment/detachment, we show analytically in an experimentally relevant parameter space that the system goes from decaying oscillations to stable limit cycle oscillations through a supercritical Hopf bifurcation. As a function of motor activity and the number of clutches, the system exhibits a wide array of dynamical states. We corroborate our analytical results with stochastic simulations of the motor-clutch system. We obtain limit cycle oscillations in the parameter regime as predicted by our model. The frequency range of oscillations in the average clutch and motor deformation compares well with experimental results.
