Herod Morgan R, Gold Sarah, Lasecka-Dykes Lidia, Wright Caroline, Ward Joseph C, McLean Thomas C, Forrest Sophie, Jackson Terry, Tuthill Tobias J, Rowlands David J, Stonehouse Nicola J
School of Molecular and Cellular Biology, Faculty of Biological Sciences and Astbury Centre for Structural Molecular Biology, University of Leeds, Leeds, United Kingdom.
The Pirbright Institute, Pirbright, Surrey, United Kingdom.
PLoS Pathog. 2017 Oct 2;13(10):e1006666. doi: 10.1371/journal.ppat.1006666. eCollection 2017 Oct.
The RNA genomes of picornaviruses are translated into single polyproteins which are subsequently cleaved into structural and non-structural protein products. For genetic economy, proteins and processing intermediates have evolved to perform distinct functions. The picornavirus precursor protein, P3, is cleaved to produce membrane-associated 3A, primer peptide 3B, protease 3Cpro and polymerase 3Dpol. Uniquely, foot-and-mouth disease virus (FMDV) encodes three similar copies of 3B (3B1-3), thus providing a convenient natural system to explore the role(s) of 3B in the processing cascade. Using a replicon system, we confirmed by genetic deletion or functional inactivation that each copy of 3B appears to function independently to prime FMDV RNA replication. However, we also show that deletion of 3B3 prevents replication and that this could be reversed by introducing mutations at the C-terminus of 3B2 that restored the natural sequence at the 3B3-3C cleavage site. In vitro translation studies showed that precursors with 3B3 deleted were rapidly cleaved to produce 3CD but that no polymerase, 3Dpol, was detected. Complementation assays, using distinguishable replicons bearing different inactivating mutations, showed that replicons with mutations within 3Dpol could be recovered by 3Dpol derived from "helper" replicons (incorporating inactivation mutations in all three copies of 3B). However, complementation was not observed when the natural 3B-3C cleavage site was altered in the "helper" replicon, again suggesting that a processing abnormality at this position prevented the production of 3Dpol. When mutations affecting polyprotein processing were introduced into an infectious clone, viable viruses were recovered but these had acquired compensatory mutations in the 3B-3C cleavage site. These mutations were shown to restore the wild-type processing characteristics when analysed in an in vitro processing assay. Overall, this study demonstrates a dual functional role of the small primer peptide 3B3, further highlighting how picornaviruses increase genetic economy.
小核糖核酸病毒的RNA基因组被翻译为单一的多聚蛋白,随后该多聚蛋白被切割成结构蛋白和非结构蛋白产物。为了实现基因经济性,蛋白质和加工中间体已经进化出执行不同功能的能力。小核糖核酸病毒前体蛋白P3被切割产生与膜相关的3A、引物肽3B、蛋白酶3Cpro和聚合酶3Dpol。独特的是,口蹄疫病毒(FMDV)编码三个相似的3B拷贝(3B1 - 3),从而提供了一个便利的天然系统来探究3B在加工级联反应中的作用。利用复制子系统,我们通过基因缺失或功能失活证实,3B的每个拷贝似乎独立发挥作用来引发FMDV RNA复制。然而,我们还表明,缺失3B3会阻止复制,而通过在3B2的C末端引入突变恢复3B3 - 3C切割位点的天然序列可以逆转这种情况。体外翻译研究表明,缺失3B3的前体蛋白会迅速被切割产生3CD,但未检测到聚合酶3Dpol。互补试验使用带有不同失活突变的可区分复制子,结果表明,3Dpol内有突变的复制子可以被源自“辅助”复制子(在所有三个3B拷贝中都包含失活突变)的3Dpol拯救。然而,当“辅助”复制子中天然的3B - 3C切割位点发生改变时,未观察到互补现象,这再次表明该位置的加工异常阻止了3Dpol的产生。当将影响多聚蛋白加工的突变引入感染性克隆时,获得了有活力的病毒,但这些病毒在3B - 3C切割位点获得了补偿性突变。在体外加工试验中分析时,这些突变显示恢复了野生型加工特征。总体而言,本研究证明了小引物肽3B3的双重功能作用,进一步突出了小核糖核酸病毒如何提高基因经济性。