| Literature DB >> 34912119 |
Keran Zhai1, Di Liang1,2, Helin Li1,3, Fangyuan Jiao1,4, Bingxiao Yan1,2, Jing Liu1,2, Ziyao Lei1,2, Li Huang1,2, Xiangyu Gong1,2, Xin Wang1, Jiashun Miao1, Yichuan Wang5, Ji-Yun Liu1, Lin Zhang6, Ertao Wang1, Yiwen Deng1, Chi-Kuang Wen1, Hongwei Guo5, Bin Han1, Zuhua He7,8.
Abstract
Pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) in plants enable them to respond to pathogens by activating the production of defence metabolites that orchestrate immune responses1-4. How the production of defence metabolites is promoted by immune receptors and coordinated with broad-spectrum resistance remains elusive. Here we identify the deubiquitinase PICI1 as an immunity hub for PTI and ETI in rice (Oryza sativa). PICI1 deubiquitinates and stabilizes methionine synthetases to activate methionine-mediated immunity principally through biosynthesis of the phytohormone ethylene. PICI1 is targeted for degradation by blast fungal effectors, including AvrPi9, to dampen PTI. Nucleotide-binding domain, leucine-rich-repeat-containing receptors (NLRs) in the plant immune system, such as PigmR, protect PICI1 from effector-mediated degradation to reboot the methionine-ethylene cascade. Natural variation in the PICI1 gene contributes to divergence in basal blast resistance between the rice subspecies indica and japonica. Thus, NLRs govern an arms race with effectors, using a competitive mode that hinges on a critical defence metabolic pathway to synchronize PTI with ETI and ensure broad-spectrum resistance.Entities:
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Year: 2021 PMID： 34912119 DOI： 10.1038/s41586-021-04219-2
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962