Editors' ChoiceCell Biology

Forced into glucose metabolism

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Science Signaling  25 May 2021:
Vol. 14, Issue 684, eabj5683
DOI: 10.1126/scisignal.abj5683

Glucose uptake through GLUT1 enables actin cytoskeletal reinforcement in response to mechanical strain.

Mechanical strain induces remodeling of the actin cytoskeleton, which is energetically costly. Salvi et al. uncovered a pathway that coupled mechanical strain to nutrient uptake. In MCF-10A breast cancer cells or MDCK epithelial cells, mechanical strain induced glucose uptake through the glucose transporter GLUT1 and increased the localization of GLUT1 at cell-cell junctions. GLUT1 bound to the cell-cell junction protein E-cadherin in MDCK cells in two- or three-dimensional culture. When exposed to force, cells reinforce the actin cytoskeleton in a process called cell stiffening. The authors found that this process required GLUT1 and glucose metabolism in MDCK cells, as assessed by enrichment of F-actin and E-cadherin in cell-cell junctions. In addition to its association with E-cadherin, the increased localization of GLUT1 to cell-cell junctions required nonmuscle myosin IIB, the scaffolding protein ankyrin G, and the interaction of ankyrin G with E-cadherin. In MDCK cells in which cell-cell junctions were transiently disrupted, reestablishment of the barrier function and cell stiffening in response to shear stress was decreased by expression of an E-cadherin mutant that could not bind to ankyrin G. Thus, the recruitment of GLUT1 to cell-cell junctions ensures glucose uptake to support cell stiffening that enables cells to resist the effects of mechanical strain.

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