Characterization of Virus-Encoded RNA Interference Suppressors in Caenorhabditis elegans
Characterization of Virus-Encoded RNA Interference Suppressors in Caenorhabditis elegans
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DOI：
10.1128/jvi.00148-13
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发表时间：
2013-05-01
影响因子：
5.4
通讯作者：
Lu, Rui
中科院分区：
文献类型：
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作者：
Guo, Xunyang;Lu, Rui
在真菌、植物和无脊椎动物中，由病毒衍生的小干扰RNA（siRNA）指导的抗病毒RNA干扰（RNAi）代表了入侵病毒必须克服以建立感染的主要抗病毒防御。作为一种反防御机制，这些宿主的病毒产生能够抑制病毒siRNA的生物发生和/或功能的不同类型的蛋白质。这种RNA介导的病毒免疫（RDVI）在线虫秀丽隐杆线虫是已知的，表现出一些独特的功能。目前，关于RNAi在C.优美的在这里，我们表明，由Flock House病毒（FHV）编码的B2蛋白的异位表达抑制了由长双链RNA（dsRNA）或基于FHV的复制子诱导的RNAi，并促进了C. elegans通过奥赛病毒感染，但对microRNA介导的RNA沉默没有活性。我们建立了一种检测C.基于通过候选蛋白质的异位表达抑制病毒复制子触发的RDVI。对于先前提出作为VSR的两种奥赛病毒蛋白中的任一种，均未检测到VSR活性。我们检测到，在已知的异源VSR，VSR活性B2的野村病毒，但不为2b的番茄无精病毒，p29的真菌感染的hypovirus，或p19的番茄丛矮病毒。我们进一步表明，与植物和昆虫不同，FHV B2主要通过干扰病毒衍生的初级siRNA的功能来抑制蠕虫RDVI。
In fungi, plants, and invertebrates, antiviral RNA interference (RNAi) directed by virus-derived small interfering RNAs (siRNAs) represents a major antiviral defense that the invading viruses have to overcome in order to establish infection. As a counterdefense mechanism, viruses of these hosts produce diverse classes of proteins capable of suppressing the biogenesis and/or function of viral siRNAs. This RNA-directed viral immunity (RDVI) in the nematode Caenorhabditis elegans is known to exhibit some unique features. Currently, little is known about viral suppression of RNAi in C. elegans. Here, we show that ectopic expression of the B2 protein encoded by Flock House virus (FHV) suppresses RNAi induced by either long double-stranded RNA (dsRNA) or an FHV-based replicon and facilitates the natural infection of C. elegans by Orsay virus but is not active against RNA silencing mediated by microRNAs. We report the development of an assay for the identification of viral suppressor of RNAi (VSR) in C. elegans based on the suppression of a viral replicon-triggered RDVI by ectopic expression of candidate proteins. No VSR activity was detected for either of the two Orsay viral proteins proposed previously as VSRs. We detected, among the known heterologous VSRs, VSR activity for B2 of Nodamura virus but not for 2b of tomato aspermy virus, p29 of fungus-infecting hypovirus, or p19 of tomato bushy stunt virus. We further show that, unlike that in plants and insects, FHV B2 suppresses worm RDVI mainly by interfering with the function of virus-derived primary siRNAs.