A Cadherin-Integrin-ECM code for presomitic mesoderm fluidity.

IF 3.6 2区生物学 Q1 DEVELOPMENTAL BIOLOGY

Development Pub Date : 2025-09-25 DOI:10.1242/dev.204874

Miriam A Genuth, Dörthe Jülich, Andrew T Ton, Sarah J Smith, Emilie Guillon, Mark D Shattuck, Corey S O'Hern, Scott A Holley

引用次数: 0

Abstract

Animal tissues exist within a continuum of fluid to solid states, and transitions between states are important for embryonic development, wound healing and cancer metastasis. Fluid to solid transitions are governed by the ratio of adhesive energy to kinetic energy. Here, we find that presomitic mesoderm solidification is driven by an intrinsic decline in cell speed along with an increase in adhesion mediated by Cadherin 2 in parallel with Fibronectin and its receptor Integrin α5. A computational model of cell-cell adhesion in the central tissue mesenchyme and cell-ECM adhesion on the tissue surface explains the observed phenotypes. Further, we identify negative feedback within the ECM as Fibronectin supports the formation of a separate layer of Fibrillin 2b matrix that inhibits solidification. These data reveal a tissue fluidity code in which solidification is promoted by Cadherin in parallel with Integrin α5 and Fibronectin, whereas negative feedback through Fibrillin 2b promotes fluidization.

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一个钙粘蛋白-整合素- ecm编码，用于体前中胚层的流动性。

动物组织存在于流体到固体状态的连续体中，状态之间的转换对胚胎发育、伤口愈合和癌症转移很重要。流体到固体的转变是由黏着能与动能之比决定的。在这里，我们发现体细胞前的中胚层凝固是由细胞速度的内在下降以及由钙粘蛋白2和纤维连接蛋白及其受体整合素α5介导的黏附增加所驱动的。中心组织间质细胞粘附和组织表面细胞- ecm粘附的计算模型解释了观察到的表型。此外，我们确定了ECM内的负反馈，因为纤维连接蛋白支持纤维蛋白2b基质的单独层的形成，从而抑制凝固。这些数据揭示了一个组织流动性代码，其中凝固由钙粘蛋白、整合素α5和纤维连接蛋白并行促进，而纤维蛋白2b的负反馈促进流化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Development 生物-发育生物学

CiteScore

6.70

自引率

4.30%

发文量

433

审稿时长

3 months

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