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Cellular forces sculpt organisms during development, while misregulation of cellular mechanics can promote disease. Here, we investigate how the actomyosin scaffold protein anillin contributes to epithelial mechanics in Xenopus laevis embryos. Increased mechanosensitive recruitment of vinculin to cell-cell junctions when anillin is overexpressed suggested that anillin promotes junctional tension. However, junctional laser ablation unexpectedly showed that junctions recoil faster when anillin is depleted and slower when anillin is overexpressed. Unifying these findings, we demonstrate that anillin regulates medial-apical actomyosin. Medial-apical laser ablation supports the conclusion that that tensile forces are stored across the apical surface of epithelial cells, and anillin promotes the tensile forces stored in this network. Finally, we show that anillin's effects on cellular mechanics impact tissue-wide mechanics. These results reveal anillin as a key regulator of epithelial mechanics and lay the groundwork for future studies on how anillin may contribute to mechanical events in development and disease.
R01 GM112794 National Institute of General Medical Sciences, R01 HD04475 Eunice Kennedy Shriver National Institute of Child Health and Human Development, R56 HL134195 National Heart, Lung, and Blood Institute, R01 GM112794 NIGMS NIH HHS , Graduate Research Fellowship National Science Foundation, Rackham Merit Fellowship Rackham Graduate School, R56 HL134195 NHLBI NIH HHS , Postdoctoral Fellowship Japan Society for the Promotion of Science , R01 HD044750 NICHD NIH HHS , Biomechanics in Regenerative Medicine Training Grant NIH HHS , Beckman Scholars Fellowship Arnold and Mabel Beckman Foundation, T32 EB003392 NIBIB NIH HHS
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