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微柱阵列的 F-肌动蛋白聚合的时空分析揭示了黏附位点之间的同步性。

Spatiotemporal analysis of F-actin polymerization with micropillar arrays reveals synchronization between adhesion sites.

机构信息

Department of Software and Information Systems Engineering, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.

Department of Genetics and Developmental Biology, Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 31096, Israel.

出版信息

Mol Biol Cell. 2024 Dec 1;35(12):br23. doi: 10.1091/mbc.E24-06-0276. Epub 2024 Oct 23.

Abstract

We repurposed micropillar arrays to quantify spatiotemporal inter-adhesion communication. Following the observation that integrin adhesions formed around pillar tops we relied on the precise repetitive spatial control of the pillars to reliably monitor F-actin dynamics in mouse embryonic fibroblasts as a model for spatiotemporal adhesion-related intracellular signaling. Using correlation-based analyses, we revealed localized information flows propagating between adjacent pillars that were integrated over space and time to synchronize the adhesion dynamics within the entire cell. Probing the mechanical regulation, we discovered that stiffer pillars or partial actomyosin contractility inhibition enhances inter-adhesion F-actin synchronization, and that inhibition of Arp2/3, but not formin, reduces synchronization. Our results suggest that adhesions can communicate and highlight the potential of using micropillar arrays as a tool to measure spatiotemporal intracellular signaling.

摘要

我们重新利用微柱阵列来量化时空间粘连通讯。观察到整合素粘连围绕柱顶形成后,我们依赖于柱的精确重复空间控制来可靠地监测作为时空粘连相关细胞内信号的模型的小鼠胚胎成纤维细胞中的 F-肌动蛋白动力学。使用基于相关的分析,我们揭示了在相邻柱子之间传播的局部信息流,这些信息流在空间和时间上被整合以在整个细胞内同步粘连动力学。探测机械调节,我们发现较硬的柱子或部分肌球蛋白收缩抑制增强了粘连之间的 F-肌动蛋白同步,并且抑制 Arp2/3,但不抑制形成蛋白,会降低同步性。我们的结果表明,粘连可以进行通讯,并强调了使用微柱阵列作为测量时空细胞内信号的工具的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5605/11656478/0358f6c74565/mbc-35-br23-g001.jpg

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