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Peer-reviewedCC BY 4.0Nature

Transcriptional activation of plant immunity by salicylic acid

  • Songwen Zhang1,2
  • Madeline Gish2
  • Huan Li2
  • Thomas R. Hinds2
  • Haibin Mao1,2
  • Moira Cornell2
  • Massi Silvetti2
  • Sydney Klucas2
  • Clint Vorauer3
  • Charlie C. Mundorff3
  • Smita Yadav2
  • Miklos Guttman3
1 more authors
  • Ning Zheng1,2
  1. 1Howard Hughes Medical Institute, University of Washington, Seattle, WA USA
  2. 2Department of Pharmacology, University of Washington, Seattle, WA USA
  3. 3Department of Medicinal Chemistry, University of Washington, Seattle, WA USA
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Abstract

The plant defence hormone salicylic acid (SA) triggers systemic acquired resistance by signalling through its receptor, NON-EXPRESSOR OF PATHOGENESIS-RELATED GENE 1 (NPR1), leading to widespread transcriptional reprogramming1,2. However, the molecular mechanism by which NPR1 senses SA and activates transcription remains unresolved. Here we show that SA stabilizes the SA-binding domain (SBD) of NPR1 and allosterically promotes its interaction with MED15A, a subunit of the Mediator complex. Leveraging the NPR1 proxiome and AlphaFold structural predictions, we identify a direct interaction between NPR1 and the kinase-inducible domain interacting (KIX) domain of MED15A. We show that recombinant NPR1 recruits MED15A in an SA-dependent manner, and that MED15A binding reciprocally enhances the affinity of NPR1 for SA. Cryo-electron microscopy and hydrogen–deuterium exchange mass spectrometry reveal that SA and the MED15A KIX domain cooperatively potentiate NPR1-SBD for ternary complex formation by stabilizing its SA-binding core via separate interfaces. We further demonstrate that NIMIN1, a repressor of the SA–NPR1 pathway, antagonizes SA signalling by competing with MED15A for the same NPR1-SBD docking site and allosterically blocking hormone binding. In line with previous genetic evidence establishing a critical role of MED15A in SA signalling, our findings provide a mechanistic resolution to the longstanding question of how SA promotes transcriptional activation during plant immune responses.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026transcriptional,
  title = {{Transcriptional activation of plant immunity by salicylic acid}},
  author = {Songwen Zhang and Madeline Gish and Huan Li and Thomas R. Hinds and Haibin Mao and Moira Cornell and Massi Silvetti and Sydney Klucas and Clint Vorauer and Charlie C. Mundorff and Smita Yadav and Miklos Guttman and Ning Zheng},
  journal = {Nature},
  year = {2026},
  month = sep,
  doi = {10.1038/s41586-026-11021-5},
  url = {https://doi.org/10.1038/s41586-026-11021-5},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Transcriptional activation of plant immunity by salicylic acid
AU  - Songwen Zhang
AU  - Madeline Gish
AU  - Huan Li
AU  - Thomas R. Hinds
AU  - Haibin Mao
AU  - Moira Cornell
AU  - Massi Silvetti
AU  - Sydney Klucas
AU  - Clint Vorauer
AU  - Charlie C. Mundorff
AU  - Smita Yadav
AU  - Miklos Guttman
AU  - Ning Zheng
PY  - 2026
DA  - 2026/09/16
JO  - Nature
DO  - 10.1038/s41586-026-11021-5
UR  - https://doi.org/10.1038/s41586-026-11021-5
AB  - The plant defence hormone salicylic acid (SA) triggers systemic acquired resistance by signalling through its receptor, NON-EXPRESSOR OF PATHOGENESIS-RELATED GENE 1 (NPR1), leading to widespread transcriptional reprogramming1,2. However, the molecular mechanism by which NPR1 senses SA and activates transcription remains unresolved. Here we show that SA stabilizes the SA-binding domain (SBD) of NPR1 and allosterically promotes its interaction with MED15A, a subunit of the Mediator complex. Leveraging the NPR1 proxiome and AlphaFold structural predictions, we identify a direct interaction between NPR1 and the kinase-inducible domain interacting (KIX) domain of MED15A. We show that recombinant NPR1 recruits MED15A in an SA-dependent manner, and that MED15A binding reciprocally enhances the affinity of NPR1 for SA. Cryo-electron microscopy and hydrogen–deuterium exchange mass spectrometry reveal that SA and the MED15A KIX domain cooperatively potentiate NPR1-SBD for ternary complex formation by stabilizing its SA-binding core via separate interfaces. We further demonstrate that NIMIN1, a repressor of the SA–NPR1 pathway, antagonizes SA signalling by competing with MED15A for the same NPR1-SBD docking site and allosterically blocking hormone binding. In line with previous genetic evidence establishing a critical role of MED15A in SA signalling, our findings provide a mechanistic resolution to the longstanding question of how SA promotes transcriptional activation during plant immune responses.
SN  - 0028-0836
SN  - 1476-4687
ER  -