F11L-mediated inhibition of RhoA-mDia signaling stimulates microtubule dynamics during Vaccinia virus infection
F11L-mediated inhibition of RhoA-mDia signaling stimulates microtubule dynamics during Vaccinia virus infection
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DOI：
10.1016/j.chom.2007.04.007
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发表时间：
2007-05-01
影响因子：
30.3
通讯作者：
Way, Michael
中科院分区：
文献类型：
--
作者：
Arakawa, Yoshilki;Cordeiro, Joao V.;Way, Michael
微管在病毒性病原体感染周期的建立过程中起着重要的作用。微管细胞骨架还促进在感染的后期有效释放新组装的后代。然而，病毒感染对微管动力学的确切影响尚不清楚。使用活细胞成像，我们表明，牛痘。病毒在感染后8小时刺激外周微管动力学的增加。感染还增加了微管尖端到达细胞皮层的频率，并减少了与其增加的动力学一致的外周微管的乙酰化。这些病毒诱导的外周微管动力学的变化是独立的GTP酶Rac和Cdc42，这是已知的未感染细胞中的微管动力学的刺激。然而，它们确实需要F11 L介导的通过GTdR RhoA及其效应物mDia的信号传导抑制。我们认为，增加外周微管动力学和皮质靶向有助于增强病毒释放。
Microtubules play an important role in the transport of viral pathogens during the establishment of their infection cycles. The microtubule cytoskeleton also facilitates efficient release of newly assembled progeny at later stages of infection. However, the precise effects of viral infection on microtubule dynamics are not understood. Using live-cell imaging, we show that vaccinia. virus stimulates increases in peripheral microtubule dynamics at 8 hr post-infection. Infection also increases the frequency with which microtubule tips reach the cell cortex and reduces the acetylation of peripheral microtubules consistent with their increased dynamics. These virus-induced changes in peripheral microtubule dynamics are independent of the GTPases Rac and Cdc42, which are known stimulators of microtubule dynamics in uninfected cells. They do, however, require F11L-mediated inhibition of signaling via the GTPase RhoA and its effector, mDia. We suggest that increases in peripheral microtubule dynamics and cortical targeting contribute to enhanced virus release.