2. Academic Validation
  3. Warm temperature suppresses plant systemic acquired resistance by intercepting N-hydroxypipecolic acid biosynthesis

Warm temperature suppresses plant systemic acquired resistance by intercepting N-hydroxypipecolic acid biosynthesis

  • Plant J. 2025 Aug;123(3):e70374. doi: 10.1111/tpj.70374.
Alyssa Shields # 1,  Lingya Yao # 2 3 4,  Christina A M Rossi 1,  Paula Collado Cordon 5 6,  Jong Hum Kim 5 6 7,  Wasan Mudher Abu AlTemen 1 8,  Sha Li 9,  Eric J R Marchetta 1,  Vanessa Shivnauth 1,  Tao Chen 9,  Sheng Yang He 5 6,  Xiu-Fang Xin 2 3,  Christian Danve M Castroverde 1
Affiliations

Affiliations

  • 1 Department of Biology, Wilfrid Laurier University, Waterloo, Ontario, N2L 3C5, Canada.
  • 2 National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai, 200032, China.
  • 3 University of Chinese Academy of Sciences, Shanghai, 200032, China.
  • 4 Shanghai Key Laboratory of Plant Molecular Sciences, College of Life Sciences, Shanghai Normal University, Shanghai, 200234, China.
  • 5 Department of Biology, Duke University, Durham, North Carolina, USA, 27708.
  • 6 Howard Hughes Medical Institute, Duke University, Durham, North Carolina, USA, 27708.
  • 7 Department of Life Sciences, Pohang University of Science and Technology, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
  • 8 Department of Biology, College of Science, University of Babylon, Babylon, Iraq.
  • 9 State Key Laboratory of Agriculture Microbiology, Huazhong Agricultural University, Wuhan, China.
  • # Contributed equally.
PMID: 40758777 DOI: 10.1111/tpj.70374
Abstract

Climate warming influences disease development by targeting critical components of the plant immune system, including pattern-triggered immunity (PTI), effector-triggered immunity (ETI) and production of the central defense hormone salicylic acid (SA) at the primary pathogen Infection site. However, it is not clear if and/or how temperature impacts systemic immunity. Here we show that pathogen-triggered systemic acquired resistance (SAR) in Arabidopsis thaliana is suppressed at elevated temperature. This was accompanied by global downregulation of SAR-induced genes at elevated temperature. Abolished SAR under warmer conditions was associated with reduced biosynthesis of the SAR metabolite N-hydroxypipecolic acid (NHP) in Arabidopsis and Other plant species (such as tomato and rapeseed), as demonstrated by downregulation of NHP biosynthetic genes (ALD1 and FMO1) and reduced NHP and pipecolic acid (Pip) levels. Although multiple SAR signals have been shown previously, exogenous NHP or Pip was sufficient to restore disease protection at elevated temperature, indicating that heat-mediated SAR suppression is due to downregulation of the NHP biosynthetic pathway. Along with ALD1 and FMO1, local and systemic expression of the SA biosynthetic gene ICS1 was also suppressed at warm temperature. Finally, we defined a transcriptional network controlling thermosensitive NHP biosynthesis via the master transcription factors CBP60g and SARD1. Our findings demonstrate that warm temperatures impact not only local but also systemic immunity by impinging on NHP biosynthesis, providing a roadmap toward engineering climate-resilient plant immune systems.

Keywords

N‐hydroxypipecolic acid; climate change; plant hormone; plant immunity; systemic acquired resistance.

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