Traction and Stress Control Formation and Motion of +1/2 Topological Defects in Epithelial Cell Monolayers.

ArXiv Pub Date : 2025-08-08
Pradip K Bera, Molly McCord, Jun Zhang, Jacob Notbohm
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Abstract

In confluent cell monolayers, patterns of cell forces and motion are systematically altered near topological defects in cell shape. In turn, defects have been proposed to alter cell density, extrusion, and invasion, but it remains unclear how the defects form and how they affect cell forces and motion. Here, we studied +1/2 defects, and, in contrast to prior studies, we observed the concurrent occurrence of both tail-to-head and head-to-tail defect motion in the same cell monolayer. We quantified the cell velocities, the tractions at the cell-substrate interface, and the stresses within the cell layer near +1/2 defects. Results revealed that both traction and stress are sources of activity and dissipation within the epithelial cell monolayer, with the direction of motion of +1/2 defects depending on whether energy is injected by stresses or tractions. Interestingly, patterns of motion, traction, stress, and energy injection near +1/2 defects existed before defect formation, suggesting that defects form as a result of spatially coordinated patterns in cell forces and motion. These findings introduce a new focus, on coordinated patterns of force and motion that lead to defect formation and motion.

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由牵引和应力驱动的能量动力学控制上皮细胞单层中 +1/2拓扑缺陷的形成和运动
在融合细胞单层中,细胞力和运动的模式在细胞形状的拓扑缺陷附近被系统地改变。反过来,缺陷被认为可以改变细胞密度、挤压和侵袭,但目前尚不清楚缺陷是如何形成的,以及它们如何影响细胞的力和运动。在这里,我们研究了+1/2缺陷,并且,与先前的研究相反,我们观察到在同一细胞单层中同时发生从头到尾和从头到尾的缺陷运动。我们量化了细胞速度,细胞-基质界面处的拉力,以及细胞层内靠近+1/2缺陷的应力。结果表明,牵引和应力都是上皮细胞单层内的活动来源,它们之间的竞争决定了细胞是注入还是消耗能量,并决定了+1/2缺陷的运动方向。有趣的是,+1/2缺陷附近的运动、牵引、应力和能量注入模式在缺陷形成之前就存在,这表明缺陷的形成是细胞力和运动的空间协调模式的结果。这些发现颠覆了目前的观点,从缺陷决定细胞力和运动到细胞力和运动的协调模式导致缺陷的形成和运动。
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