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Poster

Session: Session 1 Presenting Authors at Posters (Evens)

P-338 - A Ca2+ sensor-TIR only cascade links PAMP signaling to activate an NLR complex for stomatal immunity

Tuesday, July 15, 2025
09:55 - 11:30  
Location: Confex Hall 3
Subcellular dynamics and signaling in host-microbe interactions

    Author(s)

  • HW

    Hanling Wang

    Tsinghua University
    Beijing, Beijing, China (People's Republic)

  • JT

    Jiaxin Tan

    Tsinghua University
    Beijing, Beijing, China (People's Republic)

  • XC

    Xiulin Cui

    Tsinghua University
    Beijing, Beijing, China (People's Republic)

  • YB

    Yuhan Bai

    Tsinghua University
    Beijing, Beijing, China (People's Republic)

  • SG

    Shang Gao

    Tsinghua University
    Beijing, Beijing, China (People's Republic)

  • BS

    Brian Staskawicz

    University of California, Berkeley
    Berkeley, California, United States

  • SS

    Susheng Song

    Capital Normal University
    Berkeley, Beijing, China (People's Republic)

  • CY

    Chuangye Yan

    Tsinghua University
    Berkeley, Beijing, China (People's Republic)

    • Presenting Author(s)

  • TQ

    Tiancong Qi

    Tsinghua University
    Beijing, Beijing, China (People's Republic)

Plants swiftly close stomata upon detecting pathogen entry, a crucial defense termed stomatal immunity. The process is initiated by cell-surface pattern recognition receptors (PRRs) that perceive pathogen-associated molecular patterns (PAMPs) and evoke a series of early cellular responses including calcium ions (Ca2+) influx, and is conducted by the intracellular nucleotide-binding leucine-rich-repeat receptors (NLRs) ADR1s within an EDS1-PAD4-ADR1 module. However, the underlying mechanisms linking PRR signaling to NLRs, and how PAMP-elicited Ca2+ influx is decoded by sensors remain unclear. Here, we show that the Nicotiana benthamiana (Nb) Toll/interleukin-1 receptor (TIR)-only protein Stomatal TIR1 (NbSTIR1) produces pRib-AMP, induces EDS1-PAD4-ADR1 complex formation and mediates stomatal immunity. Structure of pathogen infection-elicited AtEDS1-AtPAD4-AtADR1-L2 complex reveals pRib-AMP binding of AtEDS1-AtPAD4 receptor and AtADR1-L2 recognition of pRib-AMP-AtPAD4-AtEDS1 for stomatal immunity. We further show that the double C2 domain protein NbISIC1 is a Ca2+ sensor, and interacts with and constrains NbSTIR1 function at basal condition. Upon pathogen infection, NbISIC1 perceives Ca2+ signals and de-represses NbSTIR1 signaling to activate stomatal immunity. Collectively, this study uncovers a de-repression mechanism linking PRR signaling to NLRs through a Ca2+ sensor/TIR-only node, and elucidates a NLR recognition mechanism of pRib-AMP-EDS1-PAD4 during innate immunity.