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Peer-reviewedCC BYCell

Salicylic acid engages central metabolic regulators SnRK1 and TOR to govern immunity by differential phosphorylation of NPR1

  • Yixuan Chen1
  • John Withers1
  • Yulin Sun2
  • Tianyuan Chen1
  • Sargis Karapetyan1
  • Jan Draken3
  • Yezi Xiang1
  • Yuzhe Yuan1
  • Sheng Yang He1
  • Wolfgang Dröge‐Laser3
  • Jing‐Ke Weng2
  • Xinnian Dong4
4 affiliations
  1. 1Department of Biology, Duke University, Box 90338, Durham, NC 27708, USA; Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA
  2. 2Institute for Plant-Human Interface, Northeastern University, Boston, MA 02115, USA; Department of Chemistry and Chemical Biology, Department of Bioengineering, Department of Chemical Engineering, Northeastern University, Boston, MA 02115, USA
  3. 3Department of Pharmaceutical Biology, Julius-von-Sachs-Institute, Julius-Maximilians-Universität Würzburg, 97082 Würzburg, Germany
  4. 4Department of Biology, Duke University, Box 90338, Durham, NC 27708, USA; Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA. Electronic address: [email protected]
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Abstract

Immunity is a delicate balance between combating infection and preserving the metabolic functions vital for host survival. However, the mechanisms by which immune responses are coordinated with cellular metabolism remain largely unknown. Here, we show that NONEXPRESSER OF PR GENES 1 (NPR1), the central plant immune regulator of salicylic acid (SA)-mediated defense responses, is controlled by a cascade of posttranslational modifications (PTMs) involving two master nutrient-sensing kinases. Under normal growth conditions, TARGET OF RAPAMYCIN (TOR) inhibits NPR1 through phosphorylation at Ser-55/59. During defense responses, elevated SA enhances SNF1-RELATED KINASE 1 (SnRK1) activity, which in turn inhibits TOR signaling and phosphorylates NPR1 at Ser-557. This phosphorylation event activates NPR1 and facilitates its subsequent PTMs. Together, our results reveal an integral role of SA (the active metabolite of aspirin) in controlling central metabolic regulators SnRK1 and TOR to coordinate immune responses and growth through antagonistic modifications of NPR1.

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Cite

BibTeXRIS
BibTeX
@article{chen2026salicylic,
  title = {{Salicylic acid engages central metabolic regulators SnRK1 and TOR to govern immunity by differential phosphorylation of NPR1}},
  author = {Yixuan Chen and John Withers and Yulin Sun and Tianyuan Chen and Sargis Karapetyan and Jan Draken and Yezi Xiang and Yuzhe Yuan and Sheng Yang He and Wolfgang Dröge‐Laser and Jing‐Ke Weng and Xinnian Dong},
  journal = {Cell},
  year = {2026},
  month = sep,
  doi = {10.1016/j.cell.2026.09.011},
  url = {https://doi.org/10.1016/j.cell.2026.09.011},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Salicylic acid engages central metabolic regulators SnRK1 and TOR to govern immunity by differential phosphorylation of NPR1
AU  - Yixuan Chen
AU  - John Withers
AU  - Yulin Sun
AU  - Tianyuan Chen
AU  - Sargis Karapetyan
AU  - Jan Draken
AU  - Yezi Xiang
AU  - Yuzhe Yuan
AU  - Sheng Yang He
AU  - Wolfgang Dröge‐Laser
AU  - Jing‐Ke Weng
AU  - Xinnian Dong
PY  - 2026
DA  - 2026/09/01
JO  - Cell
DO  - 10.1016/j.cell.2026.09.011
UR  - https://doi.org/10.1016/j.cell.2026.09.011
AB  - Immunity is a delicate balance between combating infection and preserving the metabolic functions vital for host survival. However, the mechanisms by which immune responses are coordinated with cellular metabolism remain largely unknown. Here, we show that NONEXPRESSER OF PR GENES 1 (NPR1), the central plant immune regulator of salicylic acid (SA)-mediated defense responses, is controlled by a cascade of posttranslational modifications (PTMs) involving two master nutrient-sensing kinases. Under normal growth conditions, TARGET OF RAPAMYCIN (TOR) inhibits NPR1 through phosphorylation at Ser-55/59. During defense responses, elevated SA enhances SNF1-RELATED KINASE 1 (SnRK1) activity, which in turn inhibits TOR signaling and phosphorylates NPR1 at Ser-557. This phosphorylation event activates NPR1 and facilitates its subsequent PTMs. Together, our results reveal an integral role of SA (the active metabolite of aspirin) in controlling central metabolic regulators SnRK1 and TOR to coordinate immune responses and growth through antagonistic modifications of NPR1.
SN  - 0092-8674
SN  - 1097-4172
ER  -