细胞生物学
肌球蛋白
细胞骨架
机械转化
葡萄糖转运蛋白
肌动蛋白
过剩1
生物物理学
化学
细胞
生物
生物化学
内分泌学
胰岛素
作者
Alicia M. Salvi,Jennifer Bays,Samantha Mackin,René‐Marc Mège,Kris A. DeMali
标识
DOI:10.1038/s41556-021-00677-y
摘要
The response of cells to forces is critical for their function and occurs via rearrangement of the actin cytoskeleton1. Cytoskeletal remodelling is energetically costly2,3, yet how cells signal for nutrient uptake remains undefined. Here we present evidence that force transmission increases glucose uptake by stimulating glucose transporter 1 (GLUT1). GLUT1 recruitment to and retention at sites of force transmission requires non-muscle myosin IIA-mediated contractility and ankyrin G. Ankyrin G forms a bridge between the force-transducing receptors and GLUT1. This bridge is critical for enabling cells under tension to tune glucose uptake to support remodelling of the actin cytoskeleton and formation of an epithelial barrier. Collectively, these data reveal an unexpected mechanism for how cells under tension take up nutrients and provide insight into how defects in glucose transport and mechanics might be linked.
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