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

2022; Springer Nature; Volume: 41; Issue: 18 Linguagem: Inglês

10.15252/embj.2021110521

1460-2075

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

Wheat and Barley Genetics and Pathology

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 (17K5D ), 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.