数字农科院2.0

Barley GRIK1-SnRK1 kinases subvert a viral virulence protein to upregulate antiviral RNAi and inhibit infection

文献类型： 外文期刊

作者： Jin, Huaibing;Han, Xinyun;Wang, Zhaohui;Xie, Yilin;Zhang, Kunpu;Zhao, Xiaoge;Wang, Lina;Yang, Jin;Liu, Huiyun;Ji, Xiang;Dong, Lingli;Zheng, Hongyuan;Hu, Weijuan;Liu, Yan;Wang, Xifeng;Zhou, Xueping;Zhang, Yijing;Qian, Weiqiang;Zheng, Wenming;Shen, Qianhua;Gou, Mingyue;Wang, Daowen

作者机构：

关键词： antiviral RNAi;BYDV;small RNA-degrading enzyme;SnRK1;wheat

期刊名称： EMBO JOURNAL

ISSN： 0261-4189

年卷期： 2022 年

页码：

收录情况： SCIE（2022版）

摘要： Viruses often usurp host machineries for their amplification, but it remains unclear if hosts may subvert virus proteins to regulate viral proliferation. Here, we show that the 17K protein, an important virulence factor conserved in barley yellow dwarf viruses (BYDVs) and related poleroviruses, is phosphorylated by host GRIK1-SnRK1 kinases, with the phosphorylated 17K (P17K) capable of enhancing the abundance of virus-derived small interfering RNAs (vsiRNAs) and thus antiviral RNAi. Furthermore, P17K interacts with barley small RNA-degrading nuclease 1 (HvSDN1) and impedes HvSDN1-catalyzed vsiRNA degradation. Additionally, P17K weakens the HvSDN1-HvAGO1 interaction, thus hindering HvSDN1 from accessing and degrading HvAGO1-carried vsiRNAs. Importantly, transgenic expression of 17K phosphomimetics (17K(5D)), or genome editing of SDN1, generates stable resistance to BYDV through elevating vsiRNA abundance. These data validate a novel mechanism that enhances antiviral RNAi through host subversion of a viral virulence protein to inhibit SDN1-catalyzed vsiRNA degradation and suggest new ways for engineering BYDV-resistant crops.

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