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Concurrent Session

Session: Concurrent Session: Extracellular & Intracellular non-self recognition & signaling (1)

“How not to die”: workings of an Arabidopsis TIR-NBS protein in amplifying systemic resistance

Monday, July 14, 2025
16:15 - 16:25  
Location: Room M+N

    Presenting Author(s)

  • FL

    Federica Locci

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

    • Author(s)

  • SC

    Steven Cheng

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

  • DJ

    Denis Janocha

    ZMBP, University of Tübingen
    Tuebingen, Baden-Wurttemberg, Germany

  • JF

    Judith Fliegmann

    ZMBP, University of Tübingen
    Tuebingen, Baden-Wurttemberg, Germany

  • SS

    Sara Stolze

    Max Planck Institute for Plant Breeding Research, Proteomics Group
    Koeln, Nordrhein-Westfalen, Germany

  • HN

    Hirofumi Nakagami

    Group leader
    Max Planck Institute for Plant Breeding Research
    Koeln, Nordrhein-Westfalen, Germany

  • HC

    Haitao Cui

    Shandong Agricultural University
    Taian, Shandong, China (People's Republic)

  • DL

    Dmitry Lapin (he/him/his)

    Group Leader
    Utrecht University
    Utrecht, Utrecht, Netherlands

  • TN

    Thorsten Nuernberger

    University of Tü​bingen
    Tuebingen, Baden-Wurttemberg, Germany

  • JP

    Jane Parker

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

Abstract Text:

Plants rely on cell surface-localized pattern-recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeats receptors (NLRs) to detect pathogens. Toll/interleukin-1/resistance (TIR)-domain proteins are a class of NLRs (i.e., TNLs). Many TNLs, as well as TIR-only proteins, are NAD+ hydrolysing enzymes, generating bioactive signalling molecules upon immunity activation, often leading to host cell death. These molecules define the engagement of enhanced disease susceptibility 1 (EDS1)-family heterodimers [namely, EDS1-PAD4 and EDS1-SAG101] and co-functioning “helper”-NLRs to activate and amplify immune defences. In Arabidopsis, the EDS1-PAD4 signalling branch leads to pathogen growth inhibition by consolidating the defence signalling activated by both PRRs and NLRs. In this study, we identified an Arabidopsis truncated TIR-domain protein, namely TIR-NBS 3 (TN3), which specifically interacts with PAD4 in a TIR-derived molecules dependent manner. Genetically, our results show that TN3 is involved in a specific PRR-triggered priming, as well as in enhancing pathogen resistance in distal/systemic tissues following local infection. Defective TN3 NADase activity fails to trigger TN3-PAD4 interaction, with subsequent impairment of systemic resistance. Our findings underline the importance of TIR proteins not only in inducing cell death and resistance in locally infected plant cells, but also in restricting pathogen spreading and growth to distal tissues.