Coordinated actions of NLR- assembled and glutamate receptor- like calcium channels in plant effector- triggered immunity

• 成果类型: Article
• 署名作者: Wang, Junli; Sun, Xinhua; Xiong, Fei; Lapin, Dmitry; Lee, Tak; Martin-Ramirez, Sergio; Prakken, Anna; Shen, Qiaochu; Bautor, Jaqueline; Maekawa, Takaki; Parker, Jane E.
• 署名单位: Max Planck Society; University of Cologne; Max Planck Society; Southwest University - China; Utrecht University; Wageningen University & Research; University of Michigan System; University of Michigan
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-13769
• DOI: 10.1073/pnas.2508018122
• 发表日期: 2025-09-02
• 关键词: cell-death; disease resistance; tir-domain; proteins; resistosome; DISCOVERY; responses; DEFENSE; complex

摘要

The plant immune system utilizes nucleotide-binding/leucine-rich repeat (NLR) proteins to detect pathogen virulence factors (effectors) inside host cells and transduce recognition to rapid defense. In dicotyledenous plants, pathogen activated Toll-like/interleukin-1 receptor-containing NLRs (TNLs) establish a signaling network of enhanced susceptibility 1 (EDS1)-family dimers with RPW8-type coiled-coil (CCR) domain NLRs (RNLs) to stimulate transcriptional reprogramming leading to host cell death and pathogen restriction. Evidence suggests that TNL-and EDS1-activated RNLs function as oligomeric Ca2+ permeable ion channels at the plasma membrane. However, the downstream processes for immunity execution are poorly understood. Here, we studied pathogen effector-triggered immunity conferred by Nicotiana benthamiana TNL (Roq1) which signals almost exclusively through the EDS1-senescence associated gene101 (SAG101)-N required gene 1 (NRG1) RNL module. We identify a pair of glutamate receptor-like Ca2+ ion channels (GLR2.9a and GLR2.9b) which, unlike most other pathogen-induced GLRs, are highly up-regulated by the EDS1-SAG101-NRG1 module in the TNL immune response. We show that oligomeric NRG1 Ca2+ channel activity is necessary for GLR2.9a and GLR2.9b induced expression. Consequently, GLR2.9a and GLR2.9b proteins contribute to NRG1-dependent Ca2+ accumulation in host cells, and to pathogen resistance and host cell death. We establish that GLR2.9a localizes mainly to the plasma membrane/cytoplasm whereas GLR2.9b accumulates preferentially at the nuclear envelope. The data show that transcriptionally up-regulated canonical Ca2+ ion channels GLR2.9a and GLR2.9b are a functional output of the EDS1-SAG101-NRG1 module for TNL-triggered immunity.