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Motility-Driven Glass and Jamming Transitions in Biological Tissues

机译:生物组织中的运动驱动玻璃和干扰过渡

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Cell motion inside dense tissues governs many biological processes, including embryonic development and cancer metastasis, and recent experiments suggest that these tissues exhibit collective glassy behavior. To make quantitative predictions about glass transitions in tissues, we study a self-propelled Voronoi model that simultaneously captures polarized cell motility and multibody cell-cell interactions in a confluent tissue, where there are no gaps between cells. We demonstrate that the model exhibits a jamming transition from a solidlike state to a fluidlike state that is controlled by three parameters: the single-cell motile speed, the persistence time of single-cell tracks, and a target shape index that characterizes the competition between cell-cell adhesion and cortical tension. In contrast to traditional particulate glasses, we are able to identify an experimentally accessible structural order parameter that specifies the entire jamming surface as a function of model parameters. We demonstrate that a continuum soft glassy rheology model precisely captures this transition in the limit of small persistence times and explain how it fails in the limit of large persistence times. These results provide a framework for understanding the collective solid-to-liquid transitions that have been observed in embryonic development and cancer progression, which may be associated with epithelial-to-mesenchymal transition in these tissues.
机译:细胞运动内部致密组织治理许多生物过程,包括胚胎发育和癌症转移,并且最近的实验表明这些组织表现出集体玻璃行为。为了使关于组织中的玻璃化转变进行定量预测,我们研究了一种自推进的VoronoI模型,其同时捕获偏振组织中的偏振细胞运动和多体细胞 - 细胞相互作用,其中细胞之间没有间隙。我们证明,该模型表现出从固态状态到由三个参数控制的流体状状态的干扰过渡:单细胞运动速度,单细胞轨道的持久性时间,以及表征之间的竞争的目标形状指标细胞 - 细胞粘附和皮质张力。与传统的微粒玻璃相比,我们能够识别实验可访问的结构顺序参数,该参数指定整个干扰表面作为模型参数的函数。我们表明,连续的柔软玻璃流变模型精确地捕捉到小持久时间的极限下的这种转变,并解释了它在大持久时间的极限下的失败。这些结果提供了理解在胚胎发育和癌症进展中观察到的集体固体转变的框架,这可能与这些组织中的上皮对间充质转换有关。

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