Institute for Integrated Cell-Material Sciences (WPI-iCeMS), Kyoto University, Kyoto, 606-8501, Japan.
JST PRESTO, Tokyo, 102-0075, Japan.
Nat Commun. 2018 Sep 10;9(1):3295. doi: 10.1038/s41467-018-05605-7.
In order to understand how tissue mechanics shapes animal body, it is critical to clarify how cells respond to and resist tissue stress when undergoing morphogenetic processes, such as cell rearrangement. Here, we address the question in the Drosophila wing epithelium, where anisotropic tissue tension orients cell rearrangements. We found that anisotropic tissue tension localizes actin interacting protein 1 (AIP1), a cofactor of cofilin, on the remodeling junction via cooperative binding of cofilin to F-actin. AIP1 and cofilin promote actin turnover and locally regulate the Canoe-mediated linkage between actomyosin and the junction. This mechanism is essential for cells to resist the mechanical load imposed on the remodeling junction perpendicular to the direction of tissue stretching. Thus, the present study delineates how AIP1 and cofilin achieve an optimal balance between resistance to tissue tension and morphogenesis.
为了理解组织力学如何塑造动物体，阐明细胞在经历形态发生过程（如细胞重排）时如何响应和抵抗组织应力是至关重要的。在这里，我们在果蝇翅膀上皮组织中解决了这个问题，在这个组织中，各向异性的组织张力使细胞重排定向。我们发现，各向异性的组织张力通过与 F-actin 的合作结合，将肌动蛋白相互作用蛋白 1（AIP1）定位在重塑连接点上，AIP1 是丝切蛋白的辅助因子。AIP1 和丝切蛋白促进肌动蛋白周转，并在局部调节 Canoe 介导的肌球蛋白和连接点之间的连接。这种机制对于细胞抵抗垂直于组织拉伸方向作用于重塑连接点的机械载荷是必不可少的。因此，本研究描述了 AIP1 和丝切蛋白如何在抵抗组织张力和形态发生之间达到最佳平衡。
