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A plant NLR receptor employs ABA central regulator PP2C-SnRK2 to activate antiviral immunity

文献类型： 外文期刊

作者： Huang, Shen 1 ; Wang, Chunli 1 ; Ding, Zixuan 1 ; Zhao, Yaqian 1 ; Dai, Jing 1 ; Li, Jia 1 ; Huang, Haining 1 ; Wang, Tongkai 1 ; Zhu, Min 1 ; Feng, Mingfeng 1 ; Ji, Yinghua 2 ; Zhang, Zhongkai 3 ; Tao, Xiaorong 1 ;

作者机构： 1.Nanjing Agr Univ, Dept Plant Pathol, Key Lab Plant Immun, Nanjing 210095, Peoples R China

2.Jiangsu Acad Agr Sci, Inst Plant Protect, Nanjing 210014, Peoples R China

3.Yunnan Acad Tobacco Agr Sci, Natl Tobacco Genet Engn Res Ctr, Key Lab Tobacco Biotechnol Breeding, Kunming 650021, Peoples R China

期刊名称：NATURE COMMUNICATIONS （ 影响因子：16.6； 五年影响因子：17.0 ）

ISSN：

年卷期： 2024 年 15 卷 1 期

页码：

收录情况： SCI

摘要： Defence against pathogens relies on intracellular nucleotide-binding, leucine-rich repeat immune receptors (NLRs) in plants. Hormone signaling including abscisic acid (ABA) pathways are activated by NLRs and play pivotal roles in defence against different pathogens. However, little is known about how hormone signaling pathways are activated by plant immune receptors. Here, we report that a plant NLR Sw-5b mimics the behavior of the ABA receptor and directly employs the ABA central regulator PP2C-SnRK2 complex to activate an ABA-dependent defence against viral pathogens. PP2C4 interacts with and constitutively inhibits SnRK2.3/2.4. Behaving in a similar manner as the ABA receptor, pathogen effector ligand recognition triggers the conformational change of Sw-5b NLR that enables binding to PP2C4 via the NB domain. This receptor-PP2C4 binding interferes with the interaction between PP2C4 and SnRK2.3/2.4, thereby releasing SnRK2.3/2.4 from PP2C4 inhibition to activate an ABA-specific antiviral immunity. These findings provide important insights into the activation of hormone signaling pathways by plant immune receptors. Huang et al. show how plant Sw-5b NLR mimics the ABA receptor to activate ABA-dependent antiviral immunity via the PP2C-SnRK2 complex. They reveal that Sw-5b NLR induces ABA accumulation, upregulates ABA response genes, and triggers defense against viral infections by releasing SnRK2 from PP2C inhibition.

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