利用微柱阵列对 F-肌动蛋白聚合的时空分析显示了粘附点之间的同步性。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2024-12-01 Epub Date: 2024-10-23 DOI:10.1091/mbc.E24-06-0276
Sarit Hollander, Yuanning Guo, Haguy Wolfenson, Assaf Zaritsky
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引用次数: 0

摘要

我们重新利用微柱阵列来量化粘连间的时空交流。在观察到整合素粘附围绕柱顶形成之后,我们依靠柱的精确重复空间控制来可靠地监测小鼠胚胎成纤维细胞中的 F-肌动蛋白动态,以此作为时空粘附相关胞内信号传导的模型。通过基于相关性的分析,我们揭示了相邻支柱之间传播的局部信息流,这些信息流在空间和时间上的整合使整个细胞内的粘附动态同步化。在探究机械调控时,我们发现更坚硬的支柱或部分肌动蛋白收缩力抑制会增强粘附间的 F-肌动蛋白同步,而 Arp2/3 而非甲形蛋白的抑制会降低同步性。我们的研究结果表明,粘附可以进行交流,并突出了使用微柱阵列作为测量时空细胞内信号传导的工具的潜力。[媒体:见正文]。
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Spatiotemporal analysis of F-actin polymerization with micropillar arrays reveals synchronization between adhesion sites.

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.

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