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一种缺失2b反防御蛋白基因的黄瓜花叶病毒突变体可抵御野生型毒株。

A cucumber mosaic virus mutant lacking the 2b counter-defence protein gene provides protection against wild-type strains.

作者信息

Ziebell Heiko, Payne Tina, Berry James O, Walsh John A, Carr John P

机构信息

Department of Plant Sciences, University of Cambridge, Cambridge CB2 3EA, UK.

Warwick HRI, Wellesbourne, Warwick CV35 9EF, UK.

出版信息

J Gen Virol. 2007 Oct;88(Pt 10):2862-2871. doi: 10.1099/vir.0.83138-0.

DOI:10.1099/vir.0.83138-0
PMID:17872541
Abstract

Several plant virus mutants, in which genes encoding silencing suppressor proteins have been deleted, are known to induce systemic or localized RNA silencing against themselves and other RNA molecules containing homologous sequences. Thus, it is thought that many cases of cross-protection, in which infection with a mild or asymptomatic virus mutant protects plants against challenge infection with closely related virulent viruses, can be explained by RNA silencing. We found that a cucumber mosaic virus (CMV) mutant of the subgroup IA strain Fny (Fny-CMVDelta2b), which cannot express the 2b silencing suppressor protein, cross-protects tobacco (Nicotiana tabacum) and Nicotiana benthamiana plants against disease induction by wild-type Fny-CMV. However, protection is most effective only if inoculation with Fny-CMVDelta2b and challenge inoculation with wild-type CMV occurs on the same leaf. Unexpectedly, Fny-CMVDelta2b also protected plants against infection with TC-CMV, a subgroup II strain that is not closely related to Fny-CMV. Additionally, in situ hybridization revealed that Fny-CMVDelta2b and Fny-CMV can co-exist in the same tissues but these tissues contain zones of Fny-CMVDelta2b-infected host cells from which Fny-CMV appears to be excluded. Taken together, it appears unlikely that cross-protection by Fny-CMVDelta2b occurs by induction of systemic RNA silencing against itself and homologous RNA sequences in wild-type CMV. It is more likely that protection occurs through either induction of very highly localized RNA silencing, or by competition between strains for host cells or resources.

摘要

已知几种植物病毒突变体,其编码沉默抑制蛋白的基因已被删除,会诱导针对自身以及其他含有同源序列的RNA分子的系统性或局部性RNA沉默。因此,人们认为,许多交叉保护的情况,即感染温和或无症状的病毒突变体可保护植物免受密切相关的强毒株的挑战感染,都可以用RNA沉默来解释。我们发现,IA亚组Fny株黄瓜花叶病毒(CMV)的一个突变体(Fny-CMVDelta2b),它不能表达2b沉默抑制蛋白,能交叉保护烟草(Nicotiana tabacum)和本氏烟草(Nicotiana benthamiana)植株免受野生型Fny-CMV诱导的病害。然而,只有当在同一片叶子上接种Fny-CMVDelta2b并接种野生型CMV进行挑战接种时,保护才最有效。出乎意料的是,Fny-CMVDelta2b还能保护植株免受TC-CMV的感染,TC-CMV是一种与Fny-CMV关系不密切的II亚组毒株。此外,原位杂交显示,Fny-CMVDelta2b和Fny-CMV可以在同一组织中共存,但这些组织中含有Fny-CMVDelta2b感染的宿主细胞区域,而Fny-CMV似乎被排除在外。综上所述,Fny-CMVDelta2b的交叉保护不太可能是通过诱导针对自身和野生型CMV中同源RNA序列的系统性RNA沉默来实现的。更有可能的是,保护是通过诱导非常高度局部化的RNA沉默,或者通过毒株之间对宿主细胞或资源的竞争来实现的。

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