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番茄丛矮病毒感染植物中缺陷干扰RNA介导症状减轻的分子机制表征

Characterization of the molecular mechanism of defective interfering RNA-mediated symptom attenuation in tombusvirus-infected plants.

作者信息

Havelda Z, Szittya G, Burgyán J

机构信息

Agricultural Biotechnology Center, Plant Science Institute, 2101 Gödöllö, Hungary.

出版信息

J Virol. 1998 Jul;72(7):6251-6. doi: 10.1128/JVI.72.7.6251-6256.1998.

DOI:10.1128/JVI.72.7.6251-6256.1998
PMID:9621100
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC110454/
Abstract

Different tombusviruses were able to support the replication of either homologous or heterologous defective interfering (DI) RNAs, and those infected plants usually developed typical attenuated symptoms. However, in some helper virus-DI RNA combinations the inoculated plants were necrotized, although they contained a high level of DI RNA, suggesting that the accumulation of DI RNA and the resulting suppression of genomic RNA replication were not directly responsible for the symptom attenuation. Moreover, the 19-kDa protein product of ORF 5, which is known to play a crucial role in necrotic symptom development, accumulated at the same level in the infected plants in the presence of protective homologous DI RNA and in the presence of nonprotective heterologous DI RNA. It was also demonstrated, by chimeric helper viruses, that the ability of heterologous DI RNA to protect the virus-infected plants against systemic necrosis is determined by the 5'-proximal region of the helper virus genome. The results presented suggest that DI RNA-mediated protection did not operate via the specific inhibition of 19-kDa protein expression but, more likely, DI RNAs in protective DI-helper virus combinations specifically interacted with viral products, preventing the induction of necrotic symptoms.

摘要

不同的番茄病毒能够支持同源或异源缺陷干扰(DI)RNA的复制,感染这些病毒的植物通常会出现典型的症状减轻现象。然而,在一些辅助病毒-DI RNA组合中,接种的植物会出现坏死现象,尽管它们含有高水平的DI RNA,这表明DI RNA的积累以及由此导致的基因组RNA复制抑制并非直接导致症状减轻的原因。此外,已知在坏死症状发展中起关键作用的ORF 5的19-kDa蛋白产物,在存在保护性同源DI RNA和非保护性异源DI RNA的情况下,在受感染植物中的积累水平相同。嵌合辅助病毒实验还表明,异源DI RNA保护病毒感染植物免受系统性坏死的能力取决于辅助病毒基因组的5'-近端区域。所呈现的结果表明,DI RNA介导的保护作用并非通过特异性抑制19-kDa蛋白的表达来实现,更有可能的是,保护性DI-辅助病毒组合中的DI RNA与病毒产物特异性相互作用,从而防止坏死症状的诱导。

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本文引用的文献

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