Cell cycle and mitosis progression during ZIKA virus infection: The viral non-structural protein NS5 as a master regulator of the APC/cyclosome?

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2024-02-01 DOI:10.1016/j.biochi.2024.01.016
Grégorie Lebeau , Mathilde Hoareau , Sébastien Rivière , Daed El Safadi , Christine Robert Da Silva , Pascale Krejbich-Trotot , Wildriss Viranaicken
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Abstract

Alterations in cell cycle regulation contribute to Zika virus (ZIKV)-associated pathogenesis and may have implications for the development of therapeutic avenues. As a matter of fact, ZIKV alters cell cycle progression at multiple stages, including G1, S, G2, and M phases. During a cell cycle, the progression of mitosis is particularly controlled to avoid any abnormalities in cell division. In this regard, the critical metaphase-anaphase transition is triggered by the activation of anaphase-promoting complex/cyclosome (APC/C) by its E3 ubiquitin ligase subunit Cdc20. Cdc20 recognizes substrates by interacting with a destruction box motif (D-box). Recently, the ZIKV nonstructural protein 5 (NS5), one of the most highly conserved flavivirus proteins, has been shown to localize to the centrosome in each pole and to spindle fibers during mitosis. Inducible expression of NS5 reveals an interaction of this viral factor with centrosomal proteins leading to an increase in the time required to complete mitosis. By analyzing the NS5 sequence, we discovered the presence of a D-box. Taken together, these data support the idea that, in addition to its role in viral replication, NS5 plays a critical role in the control of the cell cycle of infected cells and, more specifically, in the regulation of the mitotic spindle. Here we propose that the NS5 protein may interfere with the metaphase-anaphase progression, and thus cause the observed delay in mitosis via the regulation of APC/C.

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ZIKA病毒感染过程中的细胞周期和有丝分裂进程:病毒非结构蛋白 NS5 是 APC/细胞周期体的主调控因子?
细胞周期调控的改变是寨卡病毒(ZIKV)相关致病机制的一个因素,并可能对治疗途径的开发产生影响。事实上,寨卡病毒在多个阶段改变了细胞周期的进展,包括 G1、S、G2 和 M 期。在细胞周期中,有丝分裂的进展尤其受到控制,以避免细胞分裂出现任何异常。在这方面,关键的有丝分裂期-无丝分裂期转变是由无丝促进复合体/环体(APC/C)的 E3 泛素连接酶亚基 Cdc20 激活触发的。Cdc20 通过与破坏盒基序(D-box)相互作用来识别底物。最近的研究表明,ZIKV 非结构蛋白 5(NS5)是最高度保守的黄病毒蛋白之一,它在有丝分裂过程中定位在每极中心体和纺锤体纤维上。NS5的诱导表达揭示了这种病毒因子与中心体蛋白的相互作用,从而导致完成有丝分裂所需的时间延长。通过分析 NS5 序列,我们发现了一个 D-box 的存在。总之,这些数据支持了这样一种观点,即除了在病毒复制中发挥作用外,NS5 还在控制受感染细胞的细胞周期,更具体地说,在有丝分裂纺锤体的调控中发挥着关键作用。我们在此提出,NS5 蛋白可能会干扰有丝分裂期的进展,从而通过调节 APC/C 导致观察到的有丝分裂延迟。
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CiteScore
7.20
自引率
4.30%
发文量
567
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