Enhancing the resistance of peach fruit against Monilinia fructicola using exogenous nitric oxide by activating the gamma-aminobutyric acid shunt

Nitric oxide (NO) can induce plant disease resistance through signal transduction. The gamma-aminobutyric acid (GABA) shunt possesses different response modes for resisting different pathogens. However, the effect of the GABA shunt in NO-induced plant disease resistance is not clear. Herein, the role of the GABA shunt in the resistance of peach fruit induced by NO against Monilinia fructicola infection was investigated together with possible interaction pathways. NO treatment repressed the disease of peach fruit, increased the endogenous NO content, and enhanced the activities and gene expression of GABA shunt enzymes within 48 h, including glutamate decarboxylase (GAD), GABA transaminase (GABA-T) and succinic semialdehyde dehydrogenase (SSADH). However, the NO scavenger 2-(4-carboxyphenyl)− 4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) aggravated the disease of peach fruit, and inhibited the activities and gene expression of GABA shunt enzymes. The above results highlighted the importance of the GABA shunt in NO-induced disease resistance of peach fruit. It was noteworthy that the nitrosylated level of GAD4, GABA-T3 and SSADH was up-regulated at 6 and 12 h in NO-treated fruit compared with the control, which might be related to the enhanced GABA shunt activity. Additionally, NO treatment up-regulated the expression of glutamate receptor (PpGLR) and glutamate dehydrogenase (PpGDH), promoted Ca2+ influx, strengthened the activity of the tricarboxylic acid cycle (TCAC), and raised the ATP content and energy charge. Overall, the data indicated that NO treatment induced peach fruit disease resistance by activating the GABA shunt.