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Temperature-Dependent Survival of Turnip Crinkle Virus-Infected Arabidopsis Plants Relies on an RNA Silencing-Based Defense That Requires DCL2, AG02, and HEN1

文献类型： 外文期刊

作者： Zhang, Xiuchun 1 ; Zhang, Xiaofeng 1 ; Singh, Jasleen 1 ; Li, Dawei 3 ; Qu, Feng 1 ;

作者机构： 1.Ohio State Univ, Dept Plant Pathol, Wooster, OH USA

2.Chinese Acad Trop Agr Sci, Key Lab Biol & Genet Resources Trop Crops, Minist Agr, Inst Trop Biosci & Biotechnol, Haikou, Peoples R China

3.China Agr Univ, State Key Lab Agrobiotechnol, Coll Biol Sci, Beijing 100094, Peoples R China

关键词： gene silencing;mutants;mutations;plant diseases;plant pathogens;plant viruses;RNA interference;survival;Arabidopsis thaliana;Carmovirus;Tombusviridae;Turnip crinkle virus;Arabidopsis;Brassicaceae;Capparidales;dicotyledons;angiosperms;Spermatophyta;plants;eukaryotes;Tombusviridae;positive-sense ssRNA viruses;ssRNA viruses;RNA viruses;viruses;Carmovirus;Capparales;phytopathogens;RNAi;viruses of plants

期刊名称：JOURNAL OF VIROLOGY （ 影响因子：5.103； 五年影响因子：5.078 ）

ISSN：

年卷期：

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收录情况： SCI

摘要： While RNA silencing is a potent antiviral defense in plants, well-adapted plant viruses are known to encode suppressors of RNA silencing (VSR) that can neutralize the effectiveness of RNA silencing. As a result, most plant genes involved in antiviral silencing were identified by using debilitated viruses lacking silencing suppression capabilities. Therefore, it remains to be resolved whether RNA silencing plays a significant part in defending plants against wild-type viruses. We report here that, at a higher plant growth temperature (26 C) that permits rigorous replication of Turnip crinkle virus (TCV) in Arabidopsis, plants containing loss-of-function mutations within the Dicer-like 2 (DCL2), Argonaute 2 (AGO2), and HEN1 RNA methyltransferase genes died of TCV infection, whereas the wild-type Col-0 plants survived to produce viable seeds. To account for the critical role of DCL2 in ensuring the survival of wild-type plants, we established that higher temperature upregulates the activity of DCL2 to produce viral 22-nucleotide (nt) small interfering RNAs (vsRNAs). We further demonstrated that DCL2-produced 22-nt vsRNAs were fully capable of silencing target genes, but that this activity was suppressed by the TCV VSR. Finally, we provide additional evidence supporting the notion that TCV VSR suppresses RNA silencing through directly interacting with AGO2. Together, these results have revealed a specialized RNA silencing pathway involving DCL2, AGO2, and HEN1 that provides the host plants with a competitive edge against adapted viruses under environmental conditions that facilitates robust virus reproduction.

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