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交联和逆行流对片状伪足的形成和动力学的影响。

Influence of cross-linking and retrograde flow on formation and dynamics of lamellipodium.

机构信息

Department of Physics, Institute for Advanced Studies in Basic Sciences (IASBS), Zanjan 45137-66731, Iran.

Research Center for Basic Sciences & Modern Technologies (RBST), Institute for Advanced Studies in Basic Sciences (IASBS), Zanjan 45137-66731, Iran.

出版信息

PLoS One. 2019 Mar 21;14(3):e0213810. doi: 10.1371/journal.pone.0213810. eCollection 2019.

DOI:10.1371/journal.pone.0213810
PMID:30897104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6428246/
Abstract

The forces that arise from the actin cortex play a crucial role in determining the membrane deformation. These include protrusive forces due to actin polymerization, pulling forces due to transient attachment of actin filaments to the membrane, retrograde flow powered by contraction of actomyosin network, and adhesion to the extracellular matrix. Here we present a theoretical model for membrane deformation resulting from the feedback between the membrane shape and the forces acting on the membrane. We model the membrane as a series of beads connected by springs and determine the final steady-state shape of the membrane arising from the interplay between pushing/pulling forces of the actin network and the resisting membrane tension. We specifically investigate the effect of the gel dynamics on the spatio-temporal deformation of the membrane until a stable lamellipodium is formed. We show that the retrograde flow and the cross-linking velocity play an essential role in the final elongation of the membrane. Interestingly, in the simulations where motor-induced contractility is switched off, reduced retrograde flow results in an increase in the rate and amplitude of membrane protrusion. These simulations are consistent with experimental observations that report an enhancement in protrusion efficiency as myosin II molecular motors are inhibited.

摘要

肌动蛋白皮层产生的力在决定膜变形方面起着至关重要的作用。这些力包括肌动蛋白聚合产生的突出力、肌动蛋白丝短暂附着在膜上产生的拉力、由肌球蛋白网络收缩提供动力的逆行流动,以及与细胞外基质的黏附。在这里,我们提出了一个膜变形的理论模型,该模型源于膜形状和作用在膜上的力之间的反馈。我们将膜建模为一系列通过弹簧连接的珠子,并通过肌动蛋白网络的推/拉力和抵抗膜张力之间的相互作用来确定膜的最终稳定状态形状。我们特别研究了凝胶动力学对膜时空变形的影响,直到形成稳定的片状伪足。我们表明,逆行流动和交联速度在膜的最终伸长中起着至关重要的作用。有趣的是,在模拟中关闭了马达诱导的收缩性,降低的逆行流动导致膜突出的速率和幅度增加。这些模拟与实验观察结果一致,实验观察结果表明,当肌球蛋白 II 分子马达被抑制时,突起效率会提高。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0953/6428246/00c08ad08511/pone.0213810.g014.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0953/6428246/00c08ad08511/pone.0213810.g014.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0953/6428246/71c5e5d54db4/pone.0213810.g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0953/6428246/a275fac94277/pone.0213810.g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0953/6428246/00c08ad08511/pone.0213810.g014.jpg

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Regulation of the membrane wrapping transition of a cylindrical target by cytoskeleton adhesion.细胞骨架黏附对圆柱形靶标膜包裹转变的调控。
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