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首页> 外文期刊>Cell cycle >Human cytomegalovirus inactivates the G0/G1-APC/C ubiquitin ligase by Cdh1 dissociation.
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Human cytomegalovirus inactivates the G0/G1-APC/C ubiquitin ligase by Cdh1 dissociation.

机译：人类巨细胞病毒通过Cdh1分解使G0 / G1-APC / C泛素连接酶失活。

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摘要

The anaphase promoting complex/cyclosome (APC/C) is an E3 ubiquitin ligase that targets regulators of the cell division cycle for degradation by the 26S proteasome. Discovered as a key regulator of mitosis, the APC/C has more recently been recognized to also play a limiting role in the control of G(0) maintenance, G(1)/S-transition and DNA-replication. Human cytomegalovirus (HCMV) has been shown to interfere with cell cycle regulation at different levels. It can induce an S phase-prone proliferation program in quiescent cells but at the same time this virus directly inhibits competitive cellular DNA replication. Here we show, that human cytomegalovirus (HCMV) inactivates the G(0)/G(1) APC/C rapidly after infection of quiescent fibroblasts, resulting in the untimely stabilization of APC/C substrates. APC/C inactivation is caused by the dissociation of its positive regulator, Cdh1. Surprisingly, this dissociation is independent from known Cdh1 inhibitors, Emi1 and Cyclin A, suggesting that APC/C-Cdh1 inhibition by HCMV is directly caused by a viral protein or an intermediate cellular factor distinct from Emi1 and Cyclin A. Thus, upon infection of quiescent cells HCMV not only activates the E2F-dependent G(1)/S transcription program but also facilitates protein accumulation of APC/C substrates by rapid Cdh1 dissociation.
机译：后期促进复合物/环体（APC / C）是一种E3泛素连接酶，靶向26 S蛋白酶体降解的细胞分裂周期调控因子。作为有丝分裂的关键调节剂，APC / C最近被认为在控制G（0）维持，G（1）/ S-transition和DNA复制方面也起着限制作用。人类巨细胞病毒（HCMV）已显示出在不同水平上干扰细胞周期调节的作用。它可以在静止细胞中诱导易于发生S期的增殖程序，但与此同时，该病毒直接抑制竞争性细胞DNA复制。在这里，我们显示，人类巨细胞病毒（HCMV）感染静止的成纤维细胞后迅速失活G（0）/ G（1）APC / C，导致APC / C底物的不合时宜的稳定。 APC / C失活是由其正调节剂Cdh1的解离引起的。令人惊讶的是，这种解离独立于已知的Cdh1抑制剂Emi1和Cyclin A，这表明HCMV对APC / C-Cdh1的抑制作用是直接由不同于Emi1和Cyclin A的病毒蛋白或中间细胞因子引起的。静态细胞HCMV不仅激活E2F依赖的G（1）/ S转录程序，而且还通过快速Cdh1分解促进APC / C底物的蛋白质积累。

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