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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >EPLIN mediates linkage of the cadherin-catenin complex to F-actin and stabilizes the circumferential actin belt
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EPLIN mediates linkage of the cadherin-catenin complex to F-actin and stabilizes the circumferential actin belt

机译：EPLIN介导钙粘蛋白-连环蛋白复合物与F-肌动蛋白的连接并稳定圆周肌动蛋白带

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摘要

The cadherin-catenin complex is the major machinery for cell-cell adhesion in many animal species. This complex in general associates with actin fibers at its cytoplasmic side, organizing the adherens junction (AJ). In epithelial cells, the AJ encircles the cells near their apical surface and forms the "zonula adherens" or "adhesion belt." The mechanism as to how the cadherin-catenin complex and F-actin cooperate to generate these junctional structures, however, remains unknown. Here, we show that EPLIN (epithelial protein lost in neoplasm; also known as Lima-1), an actin-binding protein, couples with α-catenin and, in turn, links the cadherin-catenin complex to F-actin. Without EPLIN, this linkage was unable to form. When EPLIN had been depleted in epithelial cells, the adhesion belt was disorganized and converted into zipper-like junctions in which actin fibers were radially arranged. However, nonjunctional actin fibers were not particularly affected by EPLIN depletion. As EPLIN is known to have the ability to suppress actin depolymerization, our results suggest that EPLIN functions to link the cadherin-catenin complex to F-actin and simultaneously stabilizes this population of actin fibers, resulting in the establishment of the adhesion belt.
机译：钙粘蛋白-连环蛋白复合物是许多动物中细胞间粘附的主要机制。该复合物通常在其细胞质侧与肌动蛋白纤维缔合，从而组织粘附连接（AJ）。在上皮细胞中，AJ在其顶表面附近环绕细胞并形成“小带粘附”或“粘附带”。然而，关于钙粘蛋白-连环蛋白复合物和F-肌动蛋白如何协同产生这些连接结构的机制仍然未知。在这里，我们显示EPLIN（一种在肿瘤中丢失的上皮蛋白；也称为Lima-1），一种肌动蛋白结合蛋白，与α-catenin偶联，进而将钙粘蛋白-catenin复合物与F-actin连接。没有EPLIN，这种联系就无法形成。当EPLIN耗尽上皮细胞后，粘附带被破坏并转变成拉链状连接，其中肌动蛋白纤维呈放射状排列。但是，非结肌动蛋白纤维不受EPLIN消耗的影响特别大。由于已知EPLIN具有抑制肌动蛋白解聚的能力，因此我们的结果表明，EPLIN的功能是将钙粘蛋白-连环蛋白复合物连接至F-肌动蛋白，并同时稳定该肌动蛋白纤维群，从而形成粘附带。

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