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神经纤维瘤病2型肿瘤抑制因子Merlin和ERM蛋白与N-WASP相互作用并调节其肌动蛋白聚合功能。

The NF2 tumor suppressor Merlin and the ERM proteins interact with N-WASP and regulate its actin polymerization function.

作者信息

Manchanda Nitasha, Lyubimova Anna, Ho Hsin-Yi Henry, James Marianne F, Gusella James F, Ramesh Narayanaswamy, Snapper Scott B, Ramesh Vijaya

机构信息

Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA.

出版信息

J Biol Chem. 2005 Apr 1;280(13):12517-22. doi: 10.1074/jbc.C400583200. Epub 2005 Feb 7.

Abstract

The function of the NF2 tumor suppressor merlin has remained elusive despite increasing evidence for its role in actin cytoskeleton reorganization. The closely related ERM proteins (ezrin, radixin, and moesin) act as linkers between the cell membrane and cytoskeleton, and have also been implicated as active actin reorganizers. We report here that merlin and the ERMs can interact with and regulate N-WASP, a critical regulator of actin dynamics. Merlin and moesin were found to inhibit N-WASP-mediated actin assembly in vitro, a function that appears independent of their ability to bind actin. Furthermore, exogenous expression of a constitutively active ERM inhibits N-WASP-dependent Shigella tail formation, suggesting that the ERMs may function as inhibitors of N-WASP function in vivo. This novel function of merlin and the ERMs illustrates a mechanism by which these proteins directly exert their effects on actin reorganization and also provides new insight into N-WASP regulation.

摘要

尽管越来越多的证据表明NF2肿瘤抑制因子默林(merlin)在肌动蛋白细胞骨架重组中发挥作用,但其功能仍不清楚。密切相关的ERM蛋白(埃兹蛋白、根蛋白和膜突蛋白)作为细胞膜与细胞骨架之间的连接蛋白,也被认为是活跃的肌动蛋白重组因子。我们在此报告,默林和ERM蛋白可以与肌动蛋白动力学的关键调节因子N-WASP相互作用并对其进行调节。研究发现,默林和膜突蛋白在体外可抑制N-WASP介导的肌动蛋白组装,该功能似乎与其结合肌动蛋白的能力无关。此外,组成型激活的ERM蛋白的外源表达可抑制N-WASP依赖的志贺氏菌尾部形成,这表明ERM蛋白在体内可能作为N-WASP功能的抑制剂发挥作用。默林和ERM蛋白的这一新功能阐明了这些蛋白直接对肌动蛋白重组发挥作用的机制,也为N-WASP的调节提供了新的见解。

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