Mechanical forces, growth factors and the extracellular matrix all play crucial roles in cell adhesion. To understand how epidermal growth factor receptor (EGFR) impacts the mechanics of adhesion, we employed tension gauge tether (TGT) probes displaying the integrin ligand cRGDfK and quantified integrin tension. EGF exposure significantly increased spread area, cell circularity, integrated integrin tension, mechanical rupture density, radial organization and size of focal adhesions in Cos-7 cells on TGT surfaces. These findings suggest that EGFR regulates integrin tension and the spatial organization of focal adhesions. Additionally, we found that the mechanical tension threshold for outside-in integrin activation is tunable by EGFR. Parallel genetic and pharmacologic strategies demonstrated that these phenotypes are driven by ligand-dependent EGFR signaling. Our results establish a novel mechanism whereby EGFR regulates integrin activation and cell adhesion, providing control over cellular responses to the environment.

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机械力、生长因子和细胞外基质在细胞粘附中都起着至关重要的作用。为了了解表皮生长因子受体 (EGFR) 如何影响粘附机制，我们采用了显示整合素配体 cRGDfK 和量化整合素张力的张力计系链 (TGT) 探针。EGF 暴露显着增加了 TGT 表面 Co​​s-7 细胞的扩散面积、细胞圆形度、整合素张力、机械破裂密度、径向组织和粘着斑大小。这些发现表明 EGFR 调节整合素张力和粘着斑的空间组织。此外，我们发现由外向内整合素激活的机械张力阈值可由 EGFR 调节。并行的遗传和药理学策略表明，这些表型是由配体依赖性 EGFR 信号传导驱动的。我们的研究结果建立了一种新机制，EGFR 可以调节整合素激活和细胞粘附，从而控制细胞对环境的反应。

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