EPLIN mediates linkage of the cadherin-catenin complex to F-actin and stabilizes the circumferential actin belt
EPLIN mediates linkage of the cadherin-catenin complex to F-actin and stabilizes the circumferential actin belt
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DOI：
10.1073/pnas.0710504105
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发表时间：
2008-01-08
影响因子：
11.1
通讯作者：
Takeichi, Masatoshi
中科院分区：
文献类型：
--
作者：
Abe, Kentaro;Takeichi, Masatoshi
钙粘蛋白-连环蛋白复合物是许多动物细胞间粘附的主要机制。这种复合物通常与其胞质侧的肌动蛋白纤维结合，组织粘附连接（AJ）。在上皮细胞中，AJ包围靠近其顶面的细胞并形成“粘附小带”或“粘附带”。“然而，关于钙粘蛋白-连环蛋白复合物和F-肌动蛋白如何合作产生这些连接结构的机制仍然未知。在这里，我们表明，EPLIN（上皮蛋白在肿瘤中丢失，也被称为利马-1），肌动蛋白结合蛋白，夫妇与α-连环蛋白，反过来，连接钙粘蛋白-连环蛋白复合物的F-肌动蛋白。如果没有EPLIN，这种联系就无法形成。当上皮细胞中EPLIN被耗尽时，粘附带被打乱并转化为拉链样连接，其中肌动蛋白纤维呈放射状排列。然而，非连接肌动蛋白纤维没有受到EPLIN耗竭的特别影响。由于已知EPLIN具有抑制肌动蛋白解聚的能力，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到F-肌动蛋白，同时稳定该肌动蛋白纤维群，从而建立粘附带。
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 a-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.