Abstract

Nicotinamide adenine dinucleotide (NAD) is a pivotal coenzyme that has emerged as a central hub linking redox equilibrium and signal transduction in living cells. The homeostasis of NAD is required for plant growth, development, and adaption to environmental stresses. Quinolinate phosphoribosyltransferase (QPRT) is a key enzyme in NAD de novo synthesis pathway. T-DNA-based disruption ofQPRTgene is embryo lethal inArabidopsis thaliana. Therefore, to investigate the function ofQPRTin Arabidopsis, we generated transgenic plants with decreasedQPRTusing the RNA interference approach. While interference ofQPRTgene led to an impairment of NAD biosynthesis, theQPRTRNAi plants did not display distinguishable phenotypes under the optimal condition in comparison with wild-type plants. Intriguingly, they exhibited enhanced sensitivity to an avirulent strain ofPseudomonas syringaepv.tomato(Pst-avrRpt2), which was accompanied by a reduction in salicylic acid (SA) accumulation and down-regulation of pathogenesis-related genes expression as compared with the wild type. Moreover, oxidative stress marker genes includingGSTU24,OXI1,AOX1andFER1were markedly repressed in theQPRTRNAi plants. Taken together, these data emphasized the importance of QPRT in NAD biosynthesis and immunity defense, suggesting that decreased antibacterial immunity through the alteration of NAD status could be attributed to SA- and reactive oxygen species-dependent pathways.Keywords:NAD;QPRT;pathogen;pathogenesis-related genes;SA;oxidative stress