Reciprocal regulation between nicotinamide adenine dinucleotide metabolism and abscisic acid and stress response pathways in Arabidopsis

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. Author summary Nicotinamide adenine dinucleotide (NAD) is a coenzyme essential for metabolisms and signal transduction in all living organisms, but little is known about its role in ABA-mediated plant growth inhibition. Here we show that a mutation in QS gene that causes reduced level of NAD influences the ABA signal transduction in Arabidopsis, suggesting a possible conserved role of NAD in abiotic stress response in plants. In Arabidopsis, disruption of NAD homeostasis leads to ROS burst that results in a growth inhibition during exogenous ABA treatment. The ROS-mediated reduction of plant growth is fully restored by the mutation in genes encoding SnRK2 kinases, which are the core components in ABA signal transduction. A feedback repression of the QS transcription requires ABI4, which is a well-known transcription factor in the downstream of ABA signaling. Our study reveals the importance of NAD in ROS burst and plant adaption to environmental cues, and also provides insights into the unexpected interplay between NAD homeostasis and ABA-mediated plant growth inhibition.