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流体动力相互作用显著改变了肌动蛋白网络的动力学,导致长度相关损耗模量。

Hydrodynamic interactions significantly alter the dynamics of actin networks and result in a length scale dependent loss modulus.

机构信息

Department of Bioengineering, University of California, Berkeley, CA 94720, USA; Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Department of Mechanical Engineering, University of California, Berkeley, CA 94720, USA.

出版信息

J Biomech. 2021 May 7;120:110352. doi: 10.1016/j.jbiomech.2021.110352. Epub 2021 Mar 2.

Abstract

Actin, the primary component of the cytoskeleton, is the most studied semiflexible filament. Yet, the dynamics of actin filamentous network is still a subject of debate. Here we show that hydrodynamic interactions may significantly alter the time scale of actin network deformation. The alteration may be easily in the range of 2-20 fold depending on the structural conformations and scales of interest. We show that for a single fiber, hydrodynamic interactions between the cytoskeletal mesh-sized segments can change the net force by up to 7 folds. We also demonstrate that cytoskeletal relaxation times are underestimated if hydrodynamic interaction effects are ignored, but bending mode shapes are not appreciably influenced. Ignoring hydrodynamic interactions can result in up to 20-fold overestimation of shear loss modulus in the 2 μm range we investigated. Moreover, in agreement with experimental studies, our models explain a highly length scale dependent loss modulus. Taken together, our data suggest that including hydrodynamic interactions is key to proper modeling and analysis of actin dynamics at any scales and dimensions, and therefore must not be neglected in future models and experimental analyses of cytoskeletal dynamics.

摘要

肌动蛋白是细胞骨架的主要成分,也是研究最多的半柔性丝。然而,肌动蛋白丝状网络的动力学仍然是一个有争议的问题。在这里,我们表明流体动力相互作用可能会显著改变肌动蛋白网络变形的时间尺度。这种变化可能很容易在 2-20 倍之间变化,具体取决于感兴趣的结构构象和尺度。我们表明,对于单个纤维,细胞骨架网格大小的片段之间的流体动力相互作用可以使净力增加高达 7 倍。我们还证明,如果忽略流体动力相互作用的影响,细胞骨架弛豫时间会被低估,但弯曲模态形状不会受到明显影响。忽略流体动力相互作用会导致在我们研究的 2μm 范围内剪切损耗模量高估 20 倍。此外,与实验研究一致,我们的模型解释了高度依赖长度尺度的损耗模量。综上所述,我们的数据表明,在任何尺度和维度上对肌动蛋白动力学进行适当的建模和分析都必须考虑流体动力相互作用,因此在未来的细胞骨架动力学模型和实验分析中不能忽略。

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