Anillin regulates epithelial cell mechanics by structuring the medial-apical actomyosin network

eLife

Kayla M Dinshaw¹  Rachel E Stephenson²  Joseph H Shawky³  Torey R Arnold⁴  Tomohito Higashi⁴  Ann L Miller⁴  Lance A Davidson⁴  Farah Huq⁴ 

[1] Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, United States;Department of Developmental Biology, University of Pittsburgh, Pittsburgh, United States;Department of Bioengineering, University of Pittsburgh, Pittsburgh, United States;Department of Molecular Cellular and Developmental Biology, University of Michigan, Ann Arbor, United States;

关键词: anillin;    epithelium;    laser ablation;    actin;    tissue mechanics;    contractility;   

DOI  :  10.7554/eLife.39065

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown