N-hydroxypipecolic acid triggers systemic acquired resistance through extracellular NAD(P)

Qi Li, Mingxi Zhou, Shweta Chhajed, Fahong Yu, Sixue Chen, Yanping Zhang and Zhonglin Mou ()
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Qi Li: University of Florida, P.O. Box 110700
Mingxi Zhou: University of Florida, P.O. Box 110700
Shweta Chhajed: University of Florida, P.O. Box 118525
Fahong Yu: University of Florida, P.O. Box 103622
Sixue Chen: University of Mississippi
Yanping Zhang: University of Florida, P.O. Box 103622
Zhonglin Mou: University of Florida, P.O. Box 110700

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: Abstract Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant defense mechanism induced in distal systemic tissues by mobile signals generated at the primary infection site. Despite the discoveries of multiple potential mobile signals, how these signals cooperate to trigger downstream SAR signaling is unknown. Here, we show that endogenous extracellular nicotinamide adenine dinucleotide (phosphate) [eNAD(P)] accumulates systemically upon pathogen infection and that both eNAD(P) and the lectin receptor kinase (LecRK), LecRK-VI.2, are required in systemic tissues for the establishment of SAR. Moreover, putative mobile signals, e.g., N-hydroxypipecolic acid (NHP), trigger de novo systemic eNAD(P) accumulation largely through the respiratory burst oxidase homolog RBOHF-produced reactive oxygen species (ROS). Importantly, NHP-induced systemic immunity mainly depends on ROS, eNAD(P), LecRK-VI.2, and BAK1, indicating that NHP induces SAR primarily through the ROS-eNAD(P)-LecRK-VI.2/BAK1 signaling pathway. Our results suggest that mobile signals converge on eNAD(P) in systemic tissues to trigger SAR through LecRK-VI.2.

Date: 2023
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DOI: 10.1038/s41467-023-42629-0

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