Kobielak Agnieszka, Pasolli H Amalia, Fuchs Elaine
Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, 1230 York Avenue, Box 300, New York, NY 10021-6399, USA.
Nat Cell Biol. 2004 Jan;6(1):21-30. doi: 10.1038/ncb1075. Epub 2003 Nov 30.
During epithelial sheet formation, linear actin cables assemble at nascent adherens junctions. This process requires alpha-catenin and actin polymerization, although the underlying mechanism is poorly understood. Here, we show that formin-1 interacts with alpha-catenin, localizes to adherens junctions and nucleates unbranched actin filaments. Furthermore, disruption of the alpha-catenin-formin-1 interaction blocks assembly of radial actin cables and perturbs intercellular adhesion. A fusion protein of the beta-catenin-binding domain of alpha-catenin with the actin polymerization domains of formin-1 rescues formation of adherens junctions and associated actin cables in alpha-catenin-null keratinocytes. These findings provide new insight into how alpha-catenin orchestrates actin dynamics during intercellular junction formation.
在上皮细胞片层形成过程中，线性肌动蛋白束在新生的黏着连接处组装。这一过程需要α - 连环蛋白和肌动蛋白聚合，尽管其潜在机制尚不清楚。在这里，我们表明formin - 1与α - 连环蛋白相互作用，定位于黏着连接处并成核无分支的肌动蛋白丝。此外，α - 连环蛋白与formin - 1相互作用的破坏会阻止放射状肌动蛋白束的组装并扰乱细胞间黏附。α - 连环蛋白的β - 连环蛋白结合结构域与formin - 1的肌动蛋白聚合结构域的融合蛋白可挽救α - 连环蛋白缺失的角质形成细胞中黏着连接和相关肌动蛋白束的形成。这些发现为α - 连环蛋白在细胞间连接形成过程中如何协调肌动蛋白动力学提供了新的见解。
