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首页> 美国卫生研究院文献>PLoS Computational Biology >Filament turnover tunes both force generation and dissipation to control long-range flows in a model actomyosin cortex
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Filament turnover tunes both force generation and dissipation to control long-range flows in a model actomyosin cortex

机译：细丝周转可以同时调节力的产生和耗散以控制模型肌动球蛋白皮层中的远距离流动

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Actomyosin-based cortical flow is a fundamental engine for cellular morphogenesis. Cortical flows are generated by cross-linked networks of actin filaments and myosin motors, in which active stress produced by motor activity is opposed by passive resistance to network deformation. Continuous flow requires local remodeling through crosslink unbinding and and/or filament disassembly. But how local remodeling tunes stress production and dissipation, and how this in turn shapes long range flow, remains poorly understood. Here, we study a computational model for a cross-linked network with active motors based on minimal requirements for production and dissipation of contractile stress: Asymmetric filament compliance, spatial heterogeneity of motor activity, reversible cross-links and filament turnover. We characterize how the production and dissipation of network stress depend, individually, on cross-link dynamics and filament turnover, and how these dependencies combine to determine overall rates of cortical flow. Our analysis predicts that filament turnover is required to maintain active stress against external resistance and steady state flow in response to external stress. Steady state stress increases with filament lifetime up to a characteristic time τm, then decreases with lifetime above τm. Effective viscosity increases with filament lifetime up to a characteristic time τc, and then becomes independent of filament lifetime and sharply dependent on crosslink dynamics. These individual dependencies of active stress and effective viscosity define multiple regimes of steady state flow. In particular our model predicts that when filament lifetimes are shorter than both τc and τm, the dependencies of effective viscosity and steady state stress on filament turnover cancel one another, such that flow speed is insensitive to filament turnover, and shows a simple dependence on motor activity and crosslink dynamics. These results provide a framework for understanding how animal cells tune cortical flow through local control of network remodeling.
机译：基于肌动蛋白的皮层血流是细胞形态发生的基本引擎。肌动蛋白丝和肌球蛋白电机的交联网络产生了皮质流，其中由电机活动产生的主动应力与对网络变形的被动阻力相对。连续流动需要通过交联解开和/或细丝拆卸进行局部重塑。但是，局部重塑如何调整应力的产生和消散，以及这又如何影响远程流动，仍然知之甚少。在这里，我们基于产生和消除收缩应力的最低要求，研究了具有主动电机的交联网络的计算模型：不对称长丝顺应性，电机活动的空间异质性，可逆交联和长丝周转。我们表征网络应力的产生和消散如何分别依赖于交联动力学和细丝周转，以及这些依赖关系如何结合起来以确定皮质流的总速率。我们的分析预测，需要长丝周转以保持主动应力以抵抗外部阻力和响应于外部应力的稳态流动。稳态应力随着灯丝寿命（直到特征时间τm）的增加而增加，然后随着寿命超过τm的时间而减小。有效粘度随着长丝寿命的延长而增加，直到达到特征时间τc，然后才变得与长丝寿命无关，并严重依赖于交联动力学。这些单独的活动应力和有效粘度依赖性决定了稳态流动的多种状态。特别地，我们的模型预测，当灯丝寿命短于τc和τm时，有效粘度和稳态应力对灯丝周转的依赖性会相互抵消，从而流速对灯丝周转不敏感，并显示出对电机的简单依赖性。活动和交联动态。这些结果提供了一个框架，用于了解动物细胞如何通过网络重构的局部控制来调节皮层血流。

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