NAD+ deficiency primes defense metabolism via 1O2-escalated jasmonate biosynthesis in plants

Yechun Hong, Zongjun Yu, Qian Zhou, Chunyu Chen, Yuqiong Hao, Zhen Wang, Jian-Kang Zhu, Hongwei Guo and Ancheng C. Huang ()
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Yechun Hong: Southern University of Science and Technology
Zongjun Yu: Southern University of Science and Technology
Qian Zhou: Southern University of Science and Technology
Chunyu Chen: Southern University of Science and Technology
Yuqiong Hao: Southern University of Science and Technology
Zhen Wang: Anhui Agricultural University
Jian-Kang Zhu: Southern University of Science and Technology
Hongwei Guo: Southern University of Science and Technology
Ancheng C. Huang: Southern University of Science and Technology

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Nicotinamide adenine dinucleotide (NAD+) is a redox cofactor and signal central to cell metabolisms. Disrupting NAD homeostasis in plant alters growth and stress resistance, yet the underlying mechanisms remain largely unknown. Here, by combining genetics with multi-omics, we discover that NAD+ deficiency in qs-2 caused by mutation in NAD+ biosynthesis gene-Quinolinate Synthase retards growth but induces biosynthesis of defense compounds, notably aliphatic glucosinolates that confer insect resistance. The elevated defense in qs-2 is resulted from activated jasmonate biosynthesis, critically hydroperoxidation of α-linolenic acid by the 13-lipoxygenase (namely LOX2), which is escalated via the burst of chloroplastic ROS-singlet oxygen (1O2). The NAD+ deficiency-mediated JA induction and defense priming sequence in plants is recapitulated upon insect infestation, suggesting such defense mechanism operates in plant stress response. Hence, NAD homeostasis is a pivotal metabolic checkpoint that may be manipulated to navigate plant growth and defense metabolism for stress acclimation.

Date: 2024
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DOI: 10.1038/s41467-024-51114-1

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