Pseudomonas syringae infection causes metabolic changes in tomato leaves

Pathogen infection requires the reprogramming of host metabolism to assist the pathogen growth and stimulate host defense responses. Repression of photosynthesis is a common phenomenon during the pathogen infection, while the changes of primary metabolic pathways and carbohydrates are seldomly studied. This study aims to investigate the temporal changes of physiological parameters and primary metabolites in tomato leaves infected with Pseudomonas syringae pv. Tomato DC3000 (Pst DC3000). Pathogen infection triggered the reduction of pigments and starch accumulation. The production of reactive oxygen species and malondialdehyde are enhanced, and the acitvities of antioxidative enzymes are reduced after the pathogen infection. Pathogen induces the leaf cell enlargement and enhanced endoreduplication. Targeted metabolomics using GC-MS and LC-MS/MS reveals that metabolites in photosynthesis, sugar biosynthesis and TCA cycle are significantly increased between 24 and 36-h post inoculation (hpi). Overall, metabolites in photosynthesis, sugar biosynthesis and TCA cycle are more responsive to the pathogen infection than other metabolic pathways. Moreover, RNA-seq data in Pst DC3000-resistant and susceptible plants reveal that majority genes involved in Calvin cycle, photorespiration, sucrose and starch biosynthesis and TCA cycle have opposite transcriptional patterns after the pathogen infection. Our study illustrates drastic fluctuations of host primary metabolism during the bacterial pathogen infection, suggesting that metabolic engineering on photosynthesis, sugar biosynthesis and TCA cycle may enhance plant disease resistance.