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一种机械感知机制控制着纳米尺度上的质膜形状稳态。

A mechanosensing mechanism controls plasma membrane shape homeostasis at the nanoscale.

机构信息

Institute for Bioengineering of Catalonia, the Barcelona Institute of Technology (BIST), Barcelona, Spain.

Departament de Biomedicina, Unitat de Biofísica i Bioenginyeria, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, Barcelona, Spain.

出版信息

Elife. 2023 Sep 25;12:e72316. doi: 10.7554/eLife.72316.

Abstract

As cells migrate and experience forces from their surroundings, they constantly undergo mechanical deformations which reshape their plasma membrane (PM). To maintain homeostasis, cells need to detect and restore such changes, not only in terms of overall PM area and tension as previously described, but also in terms of local, nanoscale topography. Here, we describe a novel phenomenon, by which cells sense and restore mechanically induced PM nanoscale deformations. We show that cell stretch and subsequent compression reshape the PM in a way that generates local membrane evaginations in the 100 nm scale. These evaginations are recognized by I-BAR proteins, which triggers a burst of actin polymerization mediated by Rac1 and Arp2/3. The actin polymerization burst subsequently re-flattens the evagination, completing the mechanochemical feedback loop. Our results demonstrate a new mechanosensing mechanism for PM shape homeostasis, with potential applicability in different physiological scenarios.

摘要

当细胞迁移并受到周围环境的力的作用时,它们会不断经历重塑其质膜(PM)的机械变形。为了维持体内平衡,细胞需要检测和恢复这种变化,不仅要考虑到如前所述的整体 PM 面积和张力,还要考虑到局部、纳米级的地形。在这里,我们描述了一种新的现象,即细胞感知和恢复机械诱导的 PM 纳米级变形的现象。我们表明,细胞拉伸和随后的压缩以一种方式重塑 PM,在 100nm 尺度上产生局部膜凹陷。这些凹陷被 I-BAR 蛋白识别,这触发了 Rac1 和 Arp2/3 介导的肌动蛋白聚合爆发。肌动蛋白聚合爆发随后使凹陷重新变平,完成机械化学反馈环。我们的结果表明了 PM 形状动态平衡的一种新的机械感觉机制,在不同的生理场景中具有潜在的适用性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04ee/10569792/0474511f8162/elife-72316-fig4.jpg

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