近日，國際病毒學著名期刊Journal of Virology 在線刊登了中科院微生物研究所研究人員的最新研究成果“Satellite RNA-Derived Small Interfering RNA satsiR-12 Targeting the 3′ Untranslated Region of Cucumber Mosaic Virus Triggers Viral RNAs for Degradation,，”,，文章中，研究人員揭示了植物RNA沉默互作機制研究的新進展,。
RNA沉默是指在真核生物中發(fā)現(xiàn)的由小RNA（21-30nt）介導的,、以序列特異性方式引起靶標基因表達受抑的現(xiàn)象。在植物中,，除了能調控其生長發(fā)育,，RNA沉默在植物抵抗病毒的入侵中同樣起著非常重要的作用。一些植物病毒侵染常伴有衛(wèi)星RNA的復制,，并影響輔助病毒在寄主中的致病性,。
在國家重點基礎研究發(fā)展計劃（973計劃）等項目資助下，中國科學院微生物研究所植物基因組學國家重點實驗室郭惠珊研究員領導的課題組,，對植物RNA沉默在寄主植物,、輔助病毒和衛(wèi)星RNA三者的互作調控進行了深入的研究。他們在早期通過克隆黃瓜花葉病毒（CMV）衛(wèi)星RNA的小RNA,，探討了植物RNA沉默途徑對衛(wèi)星RNA的靶向作用（Du et al.,， 2007. Journal of Virology）。進一步研究發(fā)現(xiàn),，衛(wèi)星RNA通過下調CMV編碼的RNA沉默抑制子蛋白（CMV-2b）,，從而減輕CMV感染寄主的病癥（Hou et al.,， 2011. Molecular Plant Pathology）。
最近,，通過對衛(wèi)星RNA小RNA的生物學活性和功能的研究,，他們發(fā)現(xiàn)一個衛(wèi)星RNA的小RNA（satsiR-12）靶向CMV RNA 的3’UTR，引發(fā)植物依賴的RNA聚合酶RDR6的抗病毒沉默作用,；而CMV-2b蛋白對這種由satsiR-12-介導的依賴RDR6的下調病毒RNA作用具有抑制效應,；突變和野生型病毒的競爭性實驗進一步證實，在CMV自然侵染的條件下,，衛(wèi)星RNA的小RNA參與了RNA沉默調控輔助病毒RNA的表達,。
該研究在國際上首次直接證明了病原來源的小RNA參與調控病毒RNA的生物學功能，揭示了寄主-輔助病毒-衛(wèi)星RNA在RNA沉默層面上復雜的互作調控機制,，體現(xiàn)了衛(wèi)星RNA及其與輔助病毒和寄主的協(xié)同性進化,。（生物谷Bioon.com）
doi:10.1128/JVI.05806-11
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Satellite RNA-Derived Small Interfering RNA satsiR-12 Targeting the 3′ Untranslated Region of Cucumber Mosaic Virus Triggers Viral RNAs for Degradation
Hui Zhu1,2, Cheng-Guo Duan1, Wei-Na Hou1, Quan-Sheng Du1, Dian-Qiu Lv1,3, Rong-Xiang Fang1 and Hui-Shan Guo1,*
RNA silencing provides protection against RNA viruses by targeting both the helper virus and its satellite RNA (satRNA). Virus-derived small interfering RNAs (vsiRNAs) bound with Argonaute (AGO) proteins are presumed participants in the silencing process. Here, we show that a vsiRNA targeted to virus RNAs triggers the host RNA-dependent RNA polymerase 6 (RDR6)-mediated degradation of viral RNAs. We confirmed that satRNA-derived small interfering RNAs (satsiRNAs) could be associated with different AGO proteins in planta. The most frequently cloned satsiRNA, satsiR-12, was predicted to imperfectly match to Cucumber mosaic virus (CMV) RNAs in the upstream area of the 3′ untranslated region (3′ UTR). Moreover, an artificial satsiR-12 (asatsiR-12) mediated cleavage of a green fluorescent protein (GFP) sensor construct harboring the satsiR-12 target site. asatsiR-12 also mediated reduction of viral RNAs in 2b-deficient CMV (CMVΔ2b)-infected Nicotiana benthamiana. The reduction was not observed in CMVΔ2b-infected RDR6i plants, in which RDR6 was silenced. Following infection with 2b-containing CMV, the reduction in viral RNAs was not observed in plants of either genotype, indicating that the asatsiR-12-mediated reduction of viral RNAs in the presence of RDR6 was inhibited by the 2b protein. Our results suggest that satsiR-12 targeting the 3′ UTR of CMV RNAs triggered RDR6-dependent antiviral silencing. Competition experiments with wild-type CMV RNAs and anti-satsiR-12 mutant RNA1 in the presence of 2b and satRNA demonstrate the inhibitory effect of the 2b protein on the satsiR-12-related degradation of CMV RNAs, revealing a substantial suppressor function of the 2b protein in native CMV infection. Our data provide evidence for the important biological functions of satsiRNAs in homeostatic interactions among the host, virus, and satRNA in the final outcome of viral infection.
