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Shear-induced damped oscillations in an epithelium depend on actomyosin contraction and E-cadherin cell adhesion.
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
Scaling behavior in steady-state contractile actomyosin network flow
Contractile actomyosin network flows are crucial for many cellular processes
including cell division and motility, morphogenesis and transport. How local
remodeling of actin architecture tunes stress production and dissipation and
regulates large-scale network flow remains poorly understood. Here, we generate
contractile actomyosin networks with rapid turnover in vitro, by encapsulating
cytoplasmic Xenopus egg extracts into cell-sized 'water-in-oil' droplets.
Within minutes, the networks reach a dynamic steady-state with continuous
inward flow. The networks exhibit homogenous, density-independent contraction
for a wide range of physiological conditions, indicating that the
myosin-generated stress driving contraction is proportional to the effective
network viscosity. We further find that the contraction rate approximately
scales with the network turnover rate, but this relation breaks down in the
presence of excessive crosslinking or branching. Our findings suggest that
cells use diverse biochemical mechanisms to generate robust, yet tunable, actin
flows by regulating two parameters: turnover rate and network geometry
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