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p19 植物病毒 RNA 沉默抑制子的独立并行功能,是有效抑制子活性所必需的。

Independent parallel functions of p19 plant viral suppressor of RNA silencing required for effective suppressor activity.

机构信息

Agricultural Biotechnology Center, Institute for Plant Biotechnology, Plant Developmental Biology Group, Szent-Györgyi A. út 4, Gödöllő H-2100, Hungary.

出版信息

Nucleic Acids Res. 2014 Jan;42(1):599-608. doi: 10.1093/nar/gkt846. Epub 2013 Sep 22.

DOI:10.1093/nar/gkt846
PMID:24062160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3874164/
Abstract

Plant viruses ubiquitously mediate the induction of miR168 trough the activities of viral suppressors of RNA silencing (VSRs) controlling the accumulation of ARGONAUTE1 (AGO1), one of the main components of RNA silencing based host defence system. Here we used a mutant Tombusvirus p19 VSR (p19-3M) disabled in its main suppressor function, small interfering RNA (siRNA) binding, to investigate the biological role of VSR-mediated miR168 induction. Infection with the mutant virus carrying p19-3M VSR resulted in suppressed recovery phenotype despite the presence of free virus specific siRNAs. Analysis of the infected plants revealed that the mutant p19-3M VSR is able to induce miR168 level controlling the accumulation of the antiviral AGO1, and this activity is associated with the enhanced accumulation of viral RNAs. Moreover, saturation of the siRNA-binding capacity of p19 VSR mediated by defective interfering RNAs did not influence the miR168-inducing activity. Our data indicate that p19 VSR possesses two independent silencing suppressor functions, viral siRNA binding and the miR168-mediated AGO1 control, both of which are required to efficiently cope with the RNA-silencing based host defence. This finding suggests that p19 VSR protein evolved independent parallel capacities to block the host defence at multiple levels.

摘要

植物病毒通过其调控 RNA 沉默的主要成分之一——ARGONAUTE1(AGO1)积累的病毒 RNA 沉默抑制子(VSR)的活性,普遍介导 miR168 的诱导。在这里,我们使用一种突变的 Tombusvirus p19 VSR(p19-3M),其主要抑制功能(小干扰 RNA(siRNA)结合)丧失,来研究 VSR 介导的 miR168 诱导的生物学作用。尽管存在游离的病毒特异性 siRNA,但携带 p19-3M VSR 的突变病毒感染导致受抑制的恢复表型。对感染植物的分析表明,突变的 p19-3M VSR 能够诱导 miR168 水平,控制抗病毒 AGO1 的积累,并且这种活性与病毒 RNA 的积累增强有关。此外,缺陷干扰 RNA 介导的 p19 VSR 的 siRNA 结合能力饱和并不影响 miR168 诱导活性。我们的数据表明,p19 VSR 具有两种独立的沉默抑制功能,病毒 siRNA 结合和 miR168 介导的 AGO1 控制,这两者都需要有效地应对基于 RNA 沉默的宿主防御。这一发现表明,p19 VSR 蛋白进化出独立的平行能力,以在多个水平上阻断宿主防御。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/44778909cc20/gkt846f6p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/85e0e240e0b5/gkt846f1p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/d7fe40475e94/gkt846f2p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/0ed89ec9e0cd/gkt846f3p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/d92299cc44ad/gkt846f4p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/32bc2421ee8e/gkt846f5p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/44778909cc20/gkt846f6p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/85e0e240e0b5/gkt846f1p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/d7fe40475e94/gkt846f2p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/0ed89ec9e0cd/gkt846f3p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/d92299cc44ad/gkt846f4p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/32bc2421ee8e/gkt846f5p.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a2/3874164/44778909cc20/gkt846f6p.jpg

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