Department of Bioengineering, Stanford University, Stanford, United States; Department of Mechanical Engineering, Stanford University, Stanford, United States
Department of Biology, Stanford University, Stanford, United States; Department of Molecular and Cellular Physiology, Stanford University, Stanford, United States
Department of Bioengineering, Stanford University, Stanford, United States; Department of Mechanical Engineering, Stanford University, Stanford, United States; Department of Molecular and Cellular Physiology, Stanford University, Stanford, United States; The Stanford Cardiovascular Institute, Stanford University, Stanford, United States; Mechanical Engineering, University of California, Santa Barbara, United States; Biomolecular Science and Engineering, University of California, Santa Barbara, United States; Cellular and Developmental Biology, University of California, Santa Barbara, United States
Shear forces between cells occur during global changes in multicellular organization during morphogenesis and tissue growth, yet how cells sense shear forces and propagate a response across a tissue is unknown. We found that applying exogenous shear at the midline of an epithelium induced a local, short-term deformation near the shear plane, and a long-term collective oscillatory movement across the epithelium that spread from the shear-plane and gradually dampened. Inhibiting actomyosin contraction or E-cadherin trans-cell adhesion blocked oscillations, whereas stabilizing actin filaments prolonged oscillations. Combining these data with a model of epithelium mechanics supports a mechanism involving the generation of a shear-induced mechanical event at the shear plane which is then relayed across the epithelium by actomyosin contraction linked through E-cadherin. This causes an imbalance of forces in the epithelium, which is gradually dissipated through oscillatory cell movements and actin filament turnover to restore the force balance across the epithelium.
