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Shear-induced damped oscillations in an epithelium depend on actomyosin contraction and E-cadherin cell adhesion

机译:剪切诱导的上皮阻尼振荡取决于肌动球蛋白收缩和E-钙粘蛋白细胞粘附

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摘要

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.
机译:细胞之间的剪切力发生在形态发生和组织生长期间多细胞组织的整体变化期间,但是细胞如何感知剪切力并在整个组织中传播反应尚不清楚。我们发现,在上皮的中线施加外源剪切会在剪切平面附近引起局部短期变形,并在整个上皮上发生长期的集体振荡运动,该运动从剪切平面扩展并逐渐衰减。抑制肌动球蛋白收缩或E-钙粘着蛋白跨细胞粘附可阻止振荡,而稳定的肌动蛋白丝可延长振荡。将这些数据与上皮力学模型相结合可支持一种机制,该机制涉及在剪切面上产生剪切诱导的机械事件,然后通过通过E-钙粘着蛋白连接的肌动球蛋白收缩在整个上皮中传递信号。这导致上皮中的力失衡,其通过振荡性细胞运动和肌动蛋白丝周转而逐渐消散,以恢复整个上皮的力平衡。

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