Abstract
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.