Gurmessa Bekele, Ricketts Shea, Robertson-Anderson Rae M
Department of Physics and Biophysics, University of San Diego, San Diego, California.
Department of Physics and Biophysics, University of San Diego, San Diego, California.
Biophys J. 2017 Oct 3;113(7):1540-1550. doi: 10.1016/j.bpj.2017.01.012. Epub 2017 Feb 16.
We use optical tweezers microrheology and fluorescence microscopy to apply nonlinear microscale strains to entangled and cross-linked actin networks, and measure the resulting stress and actin filament deformations. We couple nonlinear stress response and relaxation to the velocities and displacements of individual fluorescent-labeled actin segments, at varying times throughout the strain and varying distances from the strain path, to determine the underlying molecular dynamics that give rise to the debated nonlinear response and stress propagation of cross-linked and entangled actin networks at the microscale. We show that initial stress stiffening arises from acceleration of strained filaments due to molecular extension along the strain, while softening and yielding is coupled to filament deceleration, halting, and recoil. We also demonstrate a surprising nonmonotonic dependence of filament deformation on cross-linker concentration. Namely, networks with no cross-links or substantial cross-links both exhibit fast initial filament velocities and reduced molecular recoil while intermediate cross-linker concentrations display reduced velocities and increased recoil. We show that these collective results are due to a balance of network elasticity and force-induced cross-linker unbinding and rebinding. We further show that cross-links dominate entanglement dynamics when the length between cross-linkers becomes smaller than the length between entanglements. In accord with recent simulations, we demonstrate that post-strain stress can be long-lived in cross-linked networks by distributing stress to a small fraction of highly strained connected filaments that span the network and sustain the load, thereby allowing the rest of the network to recoil and relax.
我们使用光镊微流变学和荧光显微镜技术,对缠结和交联的肌动蛋白网络施加非线性微尺度应变,并测量由此产生的应力和肌动蛋白丝变形。我们将非线性应力响应和松弛与单个荧光标记的肌动蛋白片段在整个应变过程中的不同时间以及距应变路径的不同距离处的速度和位移相关联,以确定在微观尺度上导致交联和缠结的肌动蛋白网络存在争议的非线性响应和应力传播的潜在分子动力学。我们表明,初始应力强化源于应变丝沿着应变方向的分子伸展导致的加速,而软化和屈服则与丝的减速、停止和回弹相关。我们还证明了丝变形对交联剂浓度存在令人惊讶的非单调依赖性。具体而言,无交联或大量交联的网络均表现出快速的初始丝速度和降低的分子回弹,而中等交联剂浓度则显示出速度降低和回弹增加。我们表明,这些总体结果是由于网络弹性与力诱导的交联剂解键和重键之间的平衡所致。我们进一步表明,当交联剂之间的长度小于缠结之间的长度时,交联主导缠结动力学。与最近的模拟结果一致,我们证明了在交联网络中,应变后的应力可以通过将应力分布到跨越网络并承受负载的一小部分高度应变的连接丝上而长期存在,从而使网络的其余部分能够回弹和松弛。