The intrinsic genetic programme of a cell is not always sufficient to explain the cell's activities. External mechanical stimuli are increasingly recognized as determinants of cell behaviour. In the epithelial folding event that constitutes the beginning of gastrulation in Drosophila, the genetic programme of the future mesoderm leads to the establishment of a contractile actomyosin network that triggers apical constriction of cells, and thereby, furrow formation. However, some cells do not constrict but instead stretch, even though they share the same genetic programme as their constricting neighbours. We show here that tissue-wide interactions force a subset of cells to expand even when an otherwise sufficient amount of apical, active actomyosin is present. Models based on contractile forces and linear-stress strain responses are not sufficient to reproduce experimental observations, but simulations in which cells behave as ductile materials with non-linear mechanical properties do. Our models show that this behaviour is an emergent property of supracellular actomyosin networks, in accordance with our experimental observations of actin reorganization within stretching cells.

中文翻译：

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机械竞争改变了内源性遗传程序的细胞解释

细胞的内在遗传程序并不总是足以解释细胞的活动。外部机械刺激日益被认为是细胞行为的决定因素。在构成果蝇胃小肠化的开始的上皮折叠事件中，未来中胚层的遗传程序导致建立收缩性肌动球蛋白网络，该网络触发细胞的顶端收缩，从而形成犁沟。但是，即使某些细胞与其收缩邻居共享相同的遗传程序，它们也不会收缩而是延伸。我们在这里显示，即使存在其他足够量的根尖，活动性肌动球蛋白，组织范围的相互作用也会迫使细胞亚群扩展。基于收缩力和线性应力应变响应的模型不足以重现实验观察结果，但是对模拟其中单元格表现为具有非线性机械特性的易延展材料的模型却不足够。我们的模型表明，根据我们在拉伸细胞内肌动蛋白重组的实验观察，这种行为是超细胞肌动球蛋白网络的新兴特性。