Actomyosin machinery endows cells with contractility at a single cell level. However, at a tissue scale, cells can show either contractile or extensile behaviour based on the direction of pushing or pulling forces due to neighbour interactions or substrate interactions. Previous studies have shown that a monolayer of fibroblasts behaves as a contractile system while a monolayer of epithelial cells or neural crest cells behaves as an extensile system. How these two contradictory sources of force generation can coexist has remained unexplained. Through a combination of experiments using MDCK (Madin Darby Canine Kidney) cells, and in-silico modeling, we uncover the mechanism behind this switch in behaviour of epithelial cell monolayers from extensile to contractile as the weakening of intercellular contacts. We find that this switch in active behaviour also promotes the buildup of tension at the cell substrate interface through an increase in actin stress fibers and higher traction forces. This in turn triggers a mechanotransductive response in vinculin translocation to focal adhesion sites and YAP (Yes-associated protein) transcription factor activation. Our studies also show that differences in extensility and contractility act to sort cells, thus determining a general mechanism for mechanobiological pattern formation during cell competition, morphogenesis and cancer progression.

中文翻译：

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组织中主动力的性质：收缩细胞如何形成可伸展的单层

肌动球蛋白机制赋予细胞单细胞水平的收缩力。然而，在组织规模上，细胞由于相邻相互作用或底物相互作用而基于推力或拉力的方向可以显示出收缩或伸展行为。先前的研究表明，成纤维细胞的单层表现为收缩系统，而上皮细胞或神经c细胞的单层表现为可拉伸系统。这两种相互矛盾的力量产生源如何共存尚不清楚。通过使用MDCK（Madin Darby犬肾）细胞的实验和计算机模拟，我们揭示了上皮细胞单层行为从可扩展性到可收缩性的转变背后的机制，这是由于细胞间接触的减弱。我们发现这种主动行为的转换还通过增加肌动蛋白应力纤维和更高的牵引力来促进细胞基质界面处张力的建立。反过来，这会触发新蛋白转运至粘着部位和YAP（是相关蛋白）转录因子激活的机械转导反应。我们的研究还表明，延展性和收缩性的差异可对细胞进行分类，从而确定了细胞竞争，形态发生和癌症进展过程中机械生物学模式形成的一般机制。反过来，这会触发新蛋白转运至粘着部位和YAP（是相关蛋白）转录因子激活的机械转导反应。我们的研究还表明，延展性和收缩性的差异可对细胞进行分类，从而确定了细胞竞争，形态发生和癌症进展过程中机械生物学模式形成的一般机制。反过来，这会触发新蛋白转运至粘着部位和YAP（是相关蛋白）转录因子激活的机械转导反应。我们的研究还表明，延展性和收缩性的差异可对细胞进行分类，从而确定了细胞竞争，形态发生和癌症进展过程中机械生物学模式形成的一般机制。