Shenzhen Key Laboratory of Plant Genetic Engineering and Molecular Design, SUSTech-PKU Institute of Plant and Food Science, Department of Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, Guangdong, China.
Institute of Advanced Biotechnology and School of Medicine, Southern University of Science and Technology, Shenzhen, 518055, China.
Nat Commun. 2024 Aug 6;15(1):6652. doi: 10.1038/s41467-024-51114-1.
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 (O). 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.
烟酰胺腺嘌呤二核苷酸（NAD）是一种氧化还原辅助因子和信号分子，是细胞代谢的核心。在植物中破坏 NAD 动态平衡会改变其生长和抗逆性，但其中的潜在机制在很大程度上仍是未知的。在这里，我们通过将遗传学与多组学相结合，发现由于 NAD 生物合成基因喹啉酸合酶突变导致 qs-2 中的 NAD 缺乏会减缓生长，但会诱导防御化合物的生物合成，特别是赋予昆虫抗性的脂溶性硫代葡萄糖苷。qs-2 中防御水平的提高是由于茉莉酸生物合成的激活，特别是由 13-脂氧合酶（即 LOX2）催化的亚麻酸的过氧氢化，这是通过质体 ROS-单线态氧（O）的爆发而加剧的。昆虫侵害后会在植物中再现 NAD 缺乏介导的 JA 诱导和防御启动序列，表明这种防御机制在植物应激反应中起作用。因此，NAD 动态平衡是一个关键的代谢检查点，可能被操纵以调整植物的生长和防御代谢以适应压力。
