Tomato sucrose transporter 2 facilitates Pseudomonas syringae proliferation via sugar efflux and repressing salicylic acid biosynthesis.

Bacterial pathogens require carbohydrates from host plants to support their proliferation, in which sugar transporters play critical roles. Sucrose transporters (SUTs) execute phloem loading, while their functions in the plant-pathogen interaction are largely unknown. Here, we pinpoint the role of SlSUT2 during Pseudomonas syringae pv tomato (Pst) DC3000 infection of tomato plants. SlSUT2 transcription is positively correlated with bacterial proliferation during Pst DC3000 infection. Knocking out SlSUT2 impairs plant growth and enhances resistance to the pathogen. The slsut2 mutant has reduced sugar contents in both the apoplast and phloem and more starch accumulation in photosynthetic leaf cells. Pst DC3000 induces the expression of the transcription factor SlMYC2, which binds to the SlSUT2 promoter and activates its expression. SlSUT2 interacts with the main phloem loading transporter SlSUT1 and boosts its accumulation on the plasma membrane, suggesting that defective sugar transport in the slsut2 mutant is possibly due to reduced SlSUT1 accumulation. Knocking out SlSUT1 increases the resistance against Pst DC3000 and reduces sugar content in both the apoplast and phloem. Transcriptome analysis reveals that the slsut2 mutant has enhanced SA biosynthesis and signaling. Taken together, our study demonstrates that Pst DC3000 utilizes tomato SlSUT2 to trigger sugar transport and repress SA-mediated resistance to support pathogen growth in plants, suggesting SlSUT2 as a potential target for disease control and resistance breeding.