Mitogen-Activated Protein Kinase Cascade and Reactive Oxygen Species Metabolism are Involved in Acibenzolar-S-Methyl-Induced Disease Resistance in Apples

Apple fruits were subjected to dipping treatment to explore the effects of acibenzolar-S-methyl (ASM) and the mitogen-activated protein kinase (MAPK) inhibitor PD98059 on lesion growth in fruits inoculated with Penicillium expansum. We investigated the roles of the MAPK cascade and reactive oxygen species metabolism in disease resistance in apples. ASM treatment inhibited lesion growth; suppressed catalase (CAT) activity; increased H2O2 content; reduced glutathione and ascorbic acid contents; and increased glutathione reductase, ascorbate peroxidase, peroxidase, superoxide dismutase, and NADPH oxidase activities. Moreover, ASM upregulated MdSOD, MdPOD, MdGR, MdAPX, MdMAPK4, MdMAPK2, and MdMAPKK1 expressions and downregulated MdCAT and MdMAPK3 expressions. PD98059 + ASM treatment increased CAT activity and MdCAT and MdMAPK3 expressions; inhibited MdSOD, MdPOD, MdGR, MdAPX, MdMAPK4, MdMAPK2, and MdMAPKK1 expressions; reduced superoxide dismutase, peroxidase, ascorbate peroxidase, and glutathione reductase activities; and reduced glutathione content in apples. These findings indicate that ASM induces disease resistance in apples by regulating the expressions of key genes involved in reactive oxygen species metabolism and the MAPK cascade.