Cells respond to mechanical strain by stiffening their actin cytoskeleton, a process that is energetically costly. Salvi et al. show that cells anticipate this cost by increasing glucose transport when subjected to mechanical strain. In canine or human epithelial cells in culture, exposure to strain caused accumulation of the glucose transporter GLUT1 at cell-cell junctions. The increase in transporters increased the uptake of glucose required for cytoskeletal stiffening. The transporters were tethered by the ankyrin G protein to E-cadherin–containing adhesion complexes at the cell junctions. Cells expressing a mutant form of E-cadherin that did not interact with ankyrin G failed to accumulate GLUT1 and were unable to form an effective epithelial barrier.
Nat Cell Biol. 23, 457 (2021).