Metabonomic Investigation of Penicillium expansum Infection of Apples and Salicylic Acid-Mediated Disease Resistance

Blue mold caused by Penicillium expansum infection results in severe postharvest deterioration of apples. Salicylic acid (SA) is an effective elicitor of fruit resistance. However, the metabolic mechanism of P. expansum infection of apples and the SA-mediated metabolic responses are still unknown. In this study, the metabolite changes during P. expansum infection of apples and SA-mediated disease resistance were explored by performing ultra-performance liquid chromatography and quadrupole-time-of-flight mass spectrometry. A total of 472 different metabolites were identified between the five groups of sample comparisons, and the correlated metabolic pathways were revealed by bioinformatics analysis. The upregulation of the tricarboxylic acid (TCA) cycle, galactose metabolism, and starch and sucrose metabolism reflected energy conversion for P. expansum invasion and fruit disease resistance. Changes in glyoxylate and dicarboxylate metabolism and carbapenem biosynthesis reflected the biosynthesis of virulence factors and secondary metabolites for fungal infection. Metabolic pathways related to apple natural disease resistance mainly included the upregulation of secondary metabolite biosynthesis and sphingolipid metabolism. SA promoted the TCA cycle, reactive oxygen metabolism, and secondary metabolite biosynthesis of apples for disease resistance. This study revealed the metabolic pathways of P. expansum infection of apples and SA-mediated disease resistance, which helps to improve the understanding of the pathogenic mechanism and disease control.