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肌动蛋白皮层的预应力和面积可压缩性决定了活细胞的黏弹响应。

Prestress and Area Compressibility of Actin Cortices Determine the Viscoelastic Response of Living Cells.

机构信息

Institute of Physical Chemistry, Georg-August-Universität Göttingen, 37077 Göttingen, Germany.

Max Planck Institute for Dynamics and Self-Organization, 37077 Göttingen, Germany.

出版信息

Phys Rev Lett. 2020 Aug 7;125(6):068101. doi: 10.1103/PhysRevLett.125.068101.

Abstract

Shape, dynamics, and viscoelastic properties of eukaryotic cells are primarily governed by a thin, reversibly cross-linked actomyosin cortex located directly beneath the plasma membrane. We obtain time-dependent rheological responses of fibroblasts and MDCK II cells from deformation-relaxation curves using an atomic force microscope to access the dependence of cortex fluidity on prestress. We introduce a viscoelastic model that treats the cell as a composite shell and assumes that relaxation of the cortex follows a power law giving access to cortical prestress, area-compressibility modulus, and the power law exponent (fluidity). Cortex fluidity is modulated by interfering with myosin activity. We find that the power law exponent of the cell cortex decreases with increasing intrinsic prestress and area-compressibility modulus, in accordance with previous finding for isolated actin networks subject to external stress. Extrapolation to zero tension returns the theoretically predicted power law exponent for transiently cross-linked polymer networks. In contrast to the widely used Hertzian mechanics, our model provides viscoelastic parameters independent of indenter geometry and compression velocity.

摘要

真核细胞的形状、动力学和黏弹性特性主要由位于质膜下的薄的、可还原交联的肌动球蛋白皮质层控制。我们使用原子力显微镜从变形-松弛曲线中获得成纤维细胞和 MDCK II 细胞的时变流变响应,以研究皮质流动性对预应力的依赖性。我们引入了一个黏弹性模型,将细胞视为复合壳,并假设皮质松弛遵循幂律,从而获得皮质预应力、面积压缩模量和幂律指数(流动性)。通过干扰肌球蛋白活性来调节皮质流动性。我们发现,随着内应力和面积压缩模量的增加,细胞皮质的幂律指数减小,这与先前对受外部应力的分离肌动蛋白网络的发现一致。外推到零张力返回理论预测的瞬态交联聚合物网络的幂律指数。与广泛使用的赫兹力学不同,我们的模型提供了与压头几何形状和压缩速度无关的黏弹性参数。

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