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Induction of filopodium formation by a WASP-related actin-depolymerizing protein N-WASP.

机译：WASP相关肌动蛋白解聚蛋白N-WASP诱导形成假单胞菌。

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摘要

Cdc42 is a small GTPase of the Rho family which regulates the formation of actin filaments to generate filopodia. Although there are several proteins such as PAK, ACK and WASP (Wiskott-Aldrich syndrome protein) that bind Cdc42 directly, none of these can account for the filopodium formation induced by Cdc42. Here we demonstrate that before it can induce filopodium formation, Cdc42 must bind a WASP-related protein, N-WASP, that is richest in neural tissues but is expressed ubiquitously. N-WASP induces extremely long actin microspikes only when co-expressed with active Cdc42, whereas WASP, which is expressed in haematopoietic cells, does not, despite the structural similarities between WASP and N-WASP. In a cell-free system, addition of active Cdc42 significantly stimulates the actin-depolymerizing activity of N-WASP, creating free barbed ends from which actin polymerization can then take place. This activation seems to be caused by exposure of N-WASP's actin-depolymerizing region induced by Cdc42 binding.
机译：Cdc42是Rho家族的一个小GTP酶，它调节肌动蛋白丝的形成以产生丝状伪足。尽管有几种蛋白质可以直接结合Cdc42，例如PAK，ACK和WASP（Wiskott-Aldrich综合征蛋白），但这些蛋白都不能解释Cdc42诱导的fi形成。在这里，我们证明了Cdc42必须诱导WASP相关蛋白N-WASP结合，然后才能诱导丝状假单胞菌形成，该蛋白在神经组织中含量最高，但随处可见。 N-WASP仅在与活性Cdc42共表达时才会诱导极长的肌动蛋白微突，而WASP和N-WASP在结构上却相似，但在造血细胞中表达的WASP却不会。在无细胞系统中，活性Cdc42的添加会显着刺激N-WASP的肌动蛋白解聚活性，产生自由的带刺末端，然后可以从中发生肌动蛋白聚合反应。这种激活似乎是由Cdc42结合诱导的N-WASP的肌动蛋白解聚区暴露引起的。

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