Department of Biology, York University, Toronto, Ontario M3J 1P3, Canada.
RNA. 2010 Jul;16(7):1402-19. doi: 10.1261/rna.2135210. Epub 2010 May 27.
RNA viruses recruit the host translational machinery by different mechanisms that depend partly on the structure of their genomes. In this regard, the plus-strand RNA genomes of several different pathogenic plant viruses do not contain traditional translation-stimulating elements, i.e., a 5'-cap structure and a 3'-poly(A) tail, and instead rely on a 3'-cap-independent translational enhancer (3'CITE) located in their 3' untranslated regions (UTRs) for efficient synthesis of viral proteins. We investigated the structure and function of the I-shaped class of 3'CITE in tombusviruses--also present in aureusviruses and carmoviruses--using biochemical and molecular approaches and we determined that it adopts a complex higher-order RNA structure that facilitates translation by binding simultaneously to both eukaryotic initiation factor (eIF) 4F and the 5' UTR of the viral genome. The specificity of 3'CITE binding to eIF4F is mediated, at least in part, through a direct interaction with its eIF4E subunit, whereas its association with the viral 5' UTR relies on complementary RNA-RNA base-pairing. We show for the first time that this tripartite 5' UTR/3'CITE/eIF4F complex forms in vitro in a translationally relevant environment and is required for recruitment of ribosomes to the 5' end of the viral RNA genome by a mechanism that shares some fundamental features with cap-dependent translation. Notably, our results demonstrate that the 3'CITE facilitates the initiation step of translation and validate a molecular model that has been proposed to explain how several different classes of 3'CITE function. Moreover, the virus-host interplay defined in this study provides insights into natural host resistance mechanisms that have been linked to 3'CITE activity.
RNA 病毒通过不同的机制招募宿主翻译机制,这些机制部分依赖于它们基因组的结构。在这方面,几种不同致病性植物病毒的正链 RNA 基因组不包含传统的翻译刺激元件,即 5'端帽结构和 3'端聚(A)尾,而是依赖于位于其 3'非翻译区(UTR)中的 3'端非依赖性翻译增强子(3'CITE)来有效地合成病毒蛋白。我们使用生化和分子方法研究了 TBSV 中的 I 型 3'CITE 的结构和功能 - 也存在于 Aureusviruses 和 Carmoviruses 中 - 并确定它采用了一种复杂的高级 RNA 结构,通过同时结合真核起始因子(eIF)4F 和病毒基因组的 5'UTR 来促进翻译。3'CITE 与 eIF4F 的特异性结合至少部分通过与 eIF4E 亚基的直接相互作用介导,而其与病毒 5'UTR 的关联依赖于互补的 RNA-RNA 碱基配对。我们首次表明,这种三部分 5'UTR/3'CITE/eIF4F 复合物在翻译相关环境中体外形成,并且需要通过与帽依赖翻译共享一些基本特征的机制将核糖体募集到病毒 RNA 基因组的 5'端。值得注意的是,我们的结果表明 3'CITE 促进了翻译的起始步骤,并验证了一种分子模型,该模型已被提出用于解释几种不同类型的 3'CITE 如何发挥作用。此外,本研究中定义的病毒-宿主相互作用提供了对与 3'CITE 活性相关的天然宿主抗性机制的深入了解。