Nicotinamide adenine dinucleotide (NAD) is an essential coenzyme that has emerged as a central hub linking redox equilibrium and signal transduction in living organisms. The homeostasis of NAD is required for plant growth, development, and adaption to environmental cues. In this study, we isolated a chilling hypersensitive Arabidopsis thaliana mutant named qs-2 and identified the causal mutation in the gene encoding quinolinate synthase (QS) critical for NAD biosynthesis. The qs-2 mutant is also hypersensitive to salt stress and abscisic acid (ABA) but resistant to drought stress. The qs-2 mutant accumulates a reduced level of NAD and over-accumulates reactive oxygen species (ROS). The ABA-hypersensitivity of qs-2 can be rescued by supplementation of NAD precursors and by mutations in the ABA signaling components SnRK2s or RBOHF. Furthermore, ABA-induced over-accumulation of ROS in the qs-2 mutant is dependent on the SnRK2s and RBOHF. The expression of QS gene is repressed directly by ABI4, a transcription factor in the ABA response pathway. Together, our findings reveal an unexpected interplay between NAD biosynthesis and ABA and stress signaling, which is critical for our understanding of the regulation of plant growth and stress responses.

烟酰胺腺嘌呤二核苷酸（NAD）是必不可少的辅酶，已成为连接氧化还原平衡和生物体信号转导的中心枢纽。NAD的体内平衡是植物生长，发育和适应环境线索所必需的。在这项研究中，我们分离了一个寒冷的超敏拟南芥突变体qs-2，并鉴定了对NAD生物合成至关重要的喹啉合酶（QS）编码基因中的因果突变。的QS-2突变体也是过敏对盐胁迫和脱落酸（ABA），但对干旱胁迫具有抗性。的QS-2突变体积聚NAD水平降低和过度积累的活性氧物种（ROS）。qs-2的ABA过敏反应可以通过补充NAD前体和ABA信号组件SnRK2s或RBOHF中的突变来拯救。此外，ABA引起的qs-2突变体中ROS的过度积累取决于SnRK2s和RBOHF。QS基因的表达直接被ABA反应途径中的转录因子ABI4抑制。总之，我们的发现揭示了NAD生物合成与ABA和胁迫信号之间的意外相互作用，这对于我们了解植物生长和胁迫响应的调控至关重要。