Department of Pathogen Molecular Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK.
FEBS Open Bio. 2015 Feb 24;5:138-46. doi: 10.1016/j.fob.2015.02.001. eCollection 2015.
Bluetongue virus (BTV) encodes a single capping protein, VP4, which catalyzes all reactions required to generate cap1 structures on nascent viral transcripts. Further, structural analysis by X-ray crystallography indicated each catalytic reaction is arranged as a discrete domain, including a nucleoside-2'-O-methyltransferase (2'-O MTase). In this study, we have exploited the structural information to identify the residues that are important for the catalytic activity of 2'-O MTase of VP4 and their influence on BTV replication. The effect of these mutations on GMP binding, guanylyltransferase (GTase) and methylase activities were analysed by a series of in vitro biochemical assays using recombinant mutant proteins; subsequently their effects on virus replication were assessed by introducing the same mutations in replicating viral genome using a reverse genetics system. Our data showed that single substitution mutations in the catalytic tetrad K-D-K-E were sufficient to abolish 2'-O MTase activity in vitro and to completely abrogate BTV replication in cells; although these mutants retained the upstream GMP binding, GTase and guanine-N7-methyltransferase activities. Mutations of the surrounding substrate-binding pocket (predicted to recruit cap0) had variable effects on in vitro VP4 capping activity. Only triple but not single substitution mutations of these residues in genome resulted in reduced virus replication kinetics. This is the first report investigating the importance of 2'-O MTase function for any member of the Reoviridae and highlights the significance of K-D-K-E tetrad and surrounding residues for the efficiency of 2'-O MTase activity and in turn, for virus fitness.
蓝舌病毒 (BTV) 编码一种单一的帽状蛋白 VP4,该蛋白催化新生病毒转录本生成帽 1 结构所需的所有反应。此外,通过 X 射线晶体学结构分析表明,每个催化反应都排列为一个离散的结构域,包括核苷-2'-O-甲基转移酶 (2'-O MTase)。在这项研究中,我们利用结构信息鉴定了对 VP4 的 2'-O MTase 催化活性重要的残基及其对 BTV 复制的影响。通过一系列使用重组突变蛋白的体外生化测定分析了这些突变对 GMP 结合、鸟苷酰转移酶 (GTase) 和甲基转移酶活性的影响;随后通过在复制病毒基因组中引入相同的突变,使用反向遗传学系统评估了它们对病毒复制的影响。我们的数据表明,催化四联体 K-D-K-E 中的单个取代突变足以完全消除体外 2'-O MTase 活性,并完全阻断细胞中的 BTV 复制;尽管这些突变体保留了上游 GMP 结合、GTase 和鸟嘌呤-N7-甲基转移酶活性。周围底物结合口袋(预测募集帽 0)的突变对体外 VP4 加帽活性有不同的影响。只有这些残基的三突变而不是单突变会导致病毒复制动力学降低。这是首次研究 Reoviridae 任何成员的 2'-O MTase 功能的重要性,并强调了 K-D-K-E 四联体和周围残基对 2'-O MTase 活性效率的重要性,进而对病毒适应性的重要性。