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Active hole formation in epithelioid tissues
Nature Physics ( IF 19.6 ) Pub Date : 2024-05-15 , DOI: 10.1038/s41567-024-02504-1
Jian-Qing Lv , Peng-Cheng Chen , Yun-Ping Chen , Hao-Yu Liu , Shi-Da Wang , Jianbo Bai , Cheng-Lin Lv , Yue Li , Yue Shao , Xi-Qiao Feng , Bo Li

The formation of holes in epithelial tissue is essential for development, but it can also be associated with epithelial barrier dysfunction and cancer progression. Here we show that active cell contraction in epithelioid monolayer tissues derived from human embryonic stem cells can spontaneously launch a morphological transition cascade consisting of hole nucleation, coalescence and network formation. Accumulated tissue-level tensile stresses drive hole expansion from isotropic round expansion to local fracture of intercellular junctions. This is followed by fast crack propagation, which is later suppressed by the self-organized supracellular actomyosin ring and accompanied by crack blunting and a fracture-to-rounding transition. During hole coalescence, we find a fracture–slip mechanism that enables layer-by-layer breaking of the multicellular bridge but without inducing excessive cell deformation. Our multiscale theory captures these experimental observations and predicts that substrate rigidity sensing and adhesion of cells compete with cellular contraction to mediate the morphological dynamics. These findings suggest that living tissues may coordinate the mechanics across molecular, cellular and tissue scales to drive topological changes while reducing the risk of mechanical damage to cells.



中文翻译:

上皮样组织中活跃的孔形成

上皮组织中孔的形成对于发育至关重要,但它也可能与上皮屏障功能障碍和癌症进展有关。在这里,我们表明,源自人类胚胎干细胞的上皮样单层组织中的主动细胞收缩可以自发地启动由空穴成核、聚结和网络形成组成的形态转变级联。累积的组织水平拉应力驱动孔从各向同性圆形扩张到细胞间连接的局部断裂。随后是快速裂纹扩展,随后被自组织的细胞上肌动球蛋白环抑制,并伴随着裂纹钝化和断裂到圆化的转变。在孔合并过程中,我们发现了一种断裂滑移机制,可以使多细胞桥逐层断裂,但不会引起过度的细胞变形。我们的多尺度理论捕获了这些实验观察结果,并预测细胞的基质刚性感应和粘附与细胞收缩竞争以介导形态动力学。这些发现表明,活体组织可以协调分子、细胞和组织尺度的力学,以驱动拓扑变化,同时降低细胞机械损伤的风险。

更新日期:2024-05-15
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