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Concurrent Session

Session: Concurrent Session: Subcellular dynamics and signaling in host-microbe interactions

Glutamate receptor-like ion channels are transcriptionally induced by the EDS1-SAG101-NRG1 node and contribute to effector-triggered immunity in Nicotiana benthamiana

Tuesday, July 15, 2025
12:40 - 12:50  
Location: Confex Hall 1+2

    Presenting Author(s)

  • JW

    Junli Wang

    Postd
    Max Planck Institute for Plant Breeding Research, Germany
    Cologne, Nordrhein-Westfalen, Germany

    • Author(s)

  • XS

    Xinhua Sun

    Southwest University
    Chongqing, Sichuan, China (People's Republic)

  • FX

    Fei Xiong

    Max Planck Institute for Plant Breeding Research, Germany
    Cologne, Nordrhein-Westfalen, Germany

  • DL

    Dmitry Lapin (he/him/his)

    Group Leader
    Utrecht University
    Utrecht, Utrecht, Netherlands

  • TL

    Tak Lee

    Max Planck Institute for Plant Breeding Research
    Koln, Nordrhein-Westfalen, Germany

  • AP

    Anna Prakken

    Cologne University
    Cologne, Nordrhein-Westfalen, Germany

  • QS

    Qiaochu Shen

    University of Michigan
    Ann Arbor, Michigan, United States

  • TM

    Takaki Maekawa

    Cologne University
    Cologne, Nordrhein-Westfalen, Germany

  • JP

    Jane Parker

    Senior Group Leader
    Department of Plant-Microbe Interactions, Max-Planck Institute for Plant Breeding Research
    Cologne, GERMANY

Abstract Text:

Plant immune systems utilizes nucleotide-binding, leucine-rich repeat (NLR) proteins to activate transcriptional defenses and induce host cell death. Several studies show that Toll/interleukin-1 receptor (TIR) NLRs (TNLs) establish a signaling network with helper NLRs containing a CCHeLo domain. However, the mechanisms by which CCHeLo -NLRs mediated cell death and triggered transcriptional defenses remain poorly understood. In this study, we show that the CCHeLo -NLR N requirement gene 1 (NRG1) branch of TNL pathways is necessary for the transcriptional upregulation of Glutamate receptor-like ion channels 2.9a/b (GLR2.9a/b) genes in Nicotiana benthamiana. CRISPR/Cas9-mediated double knockout of NbGLR2.9a and NbGLR2.9b lead to a partial loss of TNL Roq1-dependent host cell death and pathogen resistance. Interestingly, transient expression under the control of native promoters revealed that mCherry-tagged GLR2.9a localized to the plasma membrane and cytoplasm, while GFP-tagged GLR2.9b predominantly accumulated in the nucleus, respectively. Finally, we showed that Roq1-triggered Ca²⁺ influx is severely impaired in the glr2.9ab mutants. Our results support a model where oligomerized NRG1 forms a Ca2+-permeable cation channel, but it further cooperates with GLRs at host membranes to promote Ca2+ fluxes, thereby reprogramming cells for resistance and cell death. These data advance our understanding of how plants control Ca2+ fluxes in TNL-triggered immunity.