Clathrin Potentiates Vaccinia-Induced Actin Polymerization to Facilitate Viral Spread
Clathrin Potentiates Vaccinia-Induced Actin Polymerization to Facilitate Viral Spread
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DOI：
10.1016/j.chom.2012.08.002
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发表时间：
2012-09-13
影响因子：
30.3
通讯作者：
Way, Michael
中科院分区：
文献类型：
--
作者：
Humphries, Ashley C.;Dodding, Mark P.;Way, Michael
在它们的输出过程中，新组装的牛痘病毒颗粒与质膜融合，并通过诱导arp2 /3依赖性肌动蛋白聚合增强其传播。研究围绕牛痘病毒融合的事件，我们发现牛痘以依赖于网格蛋白接头AP-2的方式瞬时募集网格蛋白。网格蛋白在牛痘中的招募显著增强了病毒诱导肌动蛋白运动的能力。我们证明了网格蛋白促进病毒肌动蛋白尾部核子A36和宿主N-WASP的聚集，后者通过Arp2/3复合物激活肌动蛋白成核。增加的聚类增强了N-WASP的稳定性，导致更有效的肌动蛋白尾部起始和持续的肌动蛋白聚合。我们的观察结果揭示了网格蛋白在病毒传播过程中意想不到的作用，并对肌动蛋白聚合的调控具有重要意义。
During their egress, newly assembled vaccinia virus particles fuse with the plasma membrane and enhance their spread by inducing Arp2/3-dependent actin polymerization. Investigating the events surrounding vaccinia virus fusion, we discovered that vaccinia transiently recruits clathrin in a manner dependent on the clathrin adaptor AP-2. The recruitment of clathrin to vaccinia dramatically enhances the ability of the virus to induce actin-based motility. We demonstrate that clathrin promotes clustering of the virus actin tail nucleator A36 and host N-WASP, which activates actin nucleation through the Arp2/3 complex. Increased clustering enhances N-WASP stability, leading to more efficient actin tail initiation and sustained actin polymerization. Our observations uncover an unexpected role for clathrin during virus spread and have important implications for the regulation of actin polymerization.