Abstract: The present study was conducted to investigate the pattern of disease resistance induced by 10 mmol/L β-aminobutyric acid (BABA) treatment in postharvest peach (Prunus persica Batsch cv ‘Baifeng’) fruits and to analyze the underlying mechanism with respect to the change in redox status. The results showed that the peach fruits treated with 10 mmol/L BABA alone demonstrated remarkably higher concentrations of the endogenous reductive signaling molecule nitric oxide (NO) and higher expression levels of PpNPR1-like, PpCHI and PpGNS genes after 2 days of storage at 20 ℃ when compared with the control, accompanied by an increase in disease incidence. Meanwhile, the fruits simultaneously treated with BABA and inoculated with the pathogen Rhizopus stolonifer exhibited significantly higher expression levels of PpNPR1-like, PpCHI and PpGNS genes during the first three days of storage than did those receiving either treatment alone (P < 0.05), and maintained high levels throughout the storage period. Moreover, either BABA treatment alone or the combined treatment stimulated the accumulation of NO and simultaneously elevated the activities of glucose 6-phosphatedehydrogenase and 6-phosphogluconate dehydrogenase, which are recognized as key enzymes in the pentose phosphate pathway (PPP), thereby contributing to enhanced production of nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH) and lower contents of NADP+ and oxidized glutathione and consequently enhanced redox status. Therefore, 10 mmol/L BABA could confer peach fruits with enhanced resistance to R. stolonifera infection by activating the priming defense, thereby reducing the incidence of soft rot disease. At the same time, BABA treatment could induce the accumulation of the reductive signaling molecule and increase the activities of the key enzymes in PPP and consequently enhance the reduction potential and activate relevant transcription factors, thereby inducing the expression of PR gene.

Key words: β-aminobutyric acid, peach fruit, redox status, pentose phosphate pathway, induction of disease resistance