Barley GRIK1‐SnRK1 kinases subvert a viral virulence protein to upregulate antiviral RNAi and inhibit infection
Year: 2022
Type: article
Abstract: 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 HvSDN1catalyzed 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.
Source: The EMBO Journal
Institutions: Chinese Academy of Sciences, Institute of Genetics and Developmental Biology, State Key Laboratory of Plant Cell and Chromosome Engineering, Henan Agricultural University, Shanghai Institutes for Biological Sciences, Center for Excellence in Molecular Plant Sciences, University of Chinese Academy of Sciences, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, State Key Laboratory of Biology of Plant Diseases and Insect Pests, Peking University, State Key Laboratory of Protein and Plant Gene Research
Language: English
Topic: Plant Virus Research Studies
Subfield: Plant Science
Domain: Life Sciences
SDG: Zero hunger
Open Access status: hybrid
Estimated APC paid: $6,100
Award: G5083324737
OpenAlex ID: W4289941998
