Abstract
The response of cells to external forces is critical for their development, differentiation, and growth and occurs via rearrangement of the actin cytoskeleton. Cytoskeletal remodeling is energetically costly, yet how cells signal for nutrient uptake remains undefined. In this study, we present evidence that force signals for increased 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, a scaffolding protein known to organize membrane proteins and domains. Ankyrin G forms a bridge between the force transducing receptors and GLUT1. This bridge is critical for allowing cells under tension to tune metabolism to meet the energy demands of remodeling the actin cytoskeleton and forming a barrier against the outside environment. Collectively, these data reveal an unexpected mechanism for how cells under tension take up nutrients, thereby providing insight into how defects in glucose transport and mechanics might be linked.
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