G6PDH regulated NADPH production and reactive oxygen species metabolism to enhance disease resistance against blue mold in apple fruit by acibenzolar-S-methyl

Apple fruit were treated with 100 mg L-1 acibenzolar-S-methyl (ASM) and 100 mu M dehydroepiandrosterone (DHEA) to investigate its effect on the lesion development inoculated with Penicillium expansum. Effects of ASM on the glucose-6-phosphate dehydrogenase (G6PDH) activity, nicotinamide ademine dinucleotidephosphate (NADPH) production, and reactive oxygen species (ROS) metabolism in apple fruit were also studied. The results indicated that ASM treatment decreased the lesion development of blue mold in apple fruit. ASM treatment enhanced the content of H2O2, the activities of NADPH oxidase (NOX), superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR) and peroxidase (POD) in apple fruit. ASM treatment increased the gene expression of SOD, APX, DHAR as well as ascorbic acid (AsA) and reduced glutathione (GSH) content whereas it inhibited MDHAR expressions. The result also indicated that ASM treatment significantly inhibited CAT activity in apple fruit. In addition, the higher activity of G6PDH and content of NADPH was observed in ASM-treated apple fruit. In contrast, lesion diameter in ASM DHEA-treated apple fruit developed more quickly than the control fruit. Also, the accumulation of H2O2, NADPH, AsA and GSH were reduced by DHEA treatment while inhibiting the activities of NOX, SOD, POD, APX, GR, MDHAR and G6PDH. Gene expressions of SOD, APX and DHAR were also inhibited by DHEA treatment. These results suggest that G6PDH played a crucial role in ROS metabolism and NADPH production in apple fruit to enhance resistance against P. expansum.