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为形态发生提供动力:细胞黏附与细胞骨架界面的多尺度挑战。

Powering morphogenesis: multiscale challenges at the interface of cell adhesion and the cytoskeleton.

机构信息

Institute of Biomedical Engineering, University of Toronto, Toronto, ON M5S 3G5, Canada.

Translational Biology and Engineering Program, Ted Rogers Centre for Heart Research, University of Toronto, Toronto, ON M5S 3G5, Canada.

出版信息

Mol Biol Cell. 2022 Jul 1;33(8). doi: 10.1091/mbc.E21-09-0452.

DOI:10.1091/mbc.E21-09-0452
PMID:35696393
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9635287/
Abstract

Among the defining features of the animal kingdom is the ability of cells to change shape and move. This underlies embryonic and postembryonic development, tissue homeostasis, regeneration, and wound healing. Cell shape change and motility require linkage of the cell's force-generating machinery to the plasma membrane at cell-cell and cell-extracellular matrix junctions. Connections of the actomyosin cytoskeleton to cell-cell adherens junctions need to be both resilient and dynamic, preventing tissue disruption during the dramatic events of embryonic morphogenesis. In the past decade, new insights radically altered the earlier simple paradigm that suggested simple linear linkage via the cadherin-catenin complex as the molecular mechanism of junction-cytoskeleton interaction. In this Perspective we provide a brief overview of our current state of knowledge and then focus on selected examples highlighting what we view as the major unanswered questions in our field and the approaches that offer exciting new insights at multiple scales from atomic structure to tissue mechanics.

摘要

动物界的一个重要特征是细胞能够改变形状和移动。这是胚胎和胚胎后发育、组织内稳态、再生和伤口愈合的基础。细胞形状的改变和运动需要将细胞的力产生机制与细胞-细胞和细胞-细胞外基质连接处的质膜连接起来。肌动球蛋白细胞骨架与细胞-细胞黏附连接的连接既需要有弹性,又需要有动态性,以防止组织在胚胎形态发生的剧烈事件中破裂。在过去的十年中,新的见解彻底改变了早期的简单模式,即通过钙粘蛋白-catenin 复合物作为连接细胞骨架相互作用的分子机制,提出了简单的线性连接。在这篇观点文章中,我们简要概述了我们目前的知识状态,然后重点介绍了一些选定的例子,突出了我们认为我们领域中主要的未解决问题,以及从原子结构到组织力学的多个尺度上提供令人兴奋的新见解的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ec/9635287/a1c5abffae4b/mbc-33-pe4-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ec/9635287/8d6f7c740ae6/mbc-33-pe4-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ec/9635287/a1c5abffae4b/mbc-33-pe4-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ec/9635287/8d6f7c740ae6/mbc-33-pe4-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ec/9635287/a1c5abffae4b/mbc-33-pe4-g002.jpg

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Nat Commun. 2022 Mar 3;13(1):1146. doi: 10.1038/s41467-022-28779-7.
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Force-dependent activation of actin elongation factor mDia1 protects the cytoskeleton from mechanical damage and promotes stress fiber repair.力依赖性激活肌动蛋白伸长因子 mDia1 保护细胞骨架免受机械损伤并促进应力纤维修复。
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Micron-scale supramolecular myosin arrays help mediate cytoskeletal assembly at mature adherens junctions.
β-肾上腺素能受体通过抑制肌动球蛋白调节胚胎上皮的伸展性。
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Cell Adhesion at the Tight Junctions: New Aspects and New Functions.细胞黏附连接:新的方面和新的功能。
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