AIP1 and cofilin ensure a resistance to tissue tension and promote directional cell rearrangement.

AIP1 and cofilin ensure a resistance to tissue tension and promote directional cell rearrangement.
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DOI:
10.1038/s41467-018-05605-7
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发表时间:
2018-09-10
影响因子:
16.6
通讯作者:
Sugimura K
Sugimura K
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Ikawa K;Sugimura K

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为了理解组织力学如何塑造动物身体,关键是要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。在这里,我们解决的问题,在果蝇翅上皮,各向异性的组织张力定向细胞重排。我们发现,各向异性的组织张力定位肌动蛋白相互作用蛋白1(AIP 1),一个辅因子的cofilin,通过合作的cofilin的F-肌动蛋白结合的重塑连接。AIP 1和cofilin促进肌动蛋白周转,并局部调节肌动球蛋白和连接之间的卡诺介导的联系。这种机制对于细胞抵抗垂直于组织拉伸方向施加在重塑连接上的机械负荷是必不可少的。因此,本研究描绘了AIP 1和cofilin如何实现抵抗组织张力和形态发生之间的最佳平衡。细胞在发育过程中增殖和移动时必须抵抗或释放张力/压缩。在这里,作者表明,AIP 1与cofilin一起,促进局部肌动蛋白更新,以调节肌动球蛋白和细胞连接之间的连接,并抵抗组织拉伸施加的机械负荷。
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. Cells must resist or release tension/compression when proliferating and moving during development. Here the authors show that AIP1, together with cofilin, promotes local actin turnover to regulate linkage between actomyosin and cell junctions and resist mechanical load imposed by tissue stretching.
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