P-264 - SWEET Tactics of Plant Defense: AtSWEET12-Mediated Apoplastic Sucrose Limitation Thwarts Bacterial Pathogens

Sugar deprivation is a potent strategy that plants use to combat bacterial pathogens. The role of SUGARS WILL EVENTUALLY BE EXPORTED TRANSPORTERS (SWEETs) in plant defense via ‘apoplasmic sugar signaling’ has been well conceived, but their function in ‘apoplasmic sugar limitation and pathogen starvation’ remains unclear. Through reverse genetic screening of Arabidopsis thaliana AtSWEET mutants, we identified a few members of clade III family involved in defense against both host and nonhost Pseudomonas syringae pathogens. Functional analysis using mutant, complementation, and overexpression lines, along with sucrose transport assays in yeast and Arabidopsis protoplasts, revealed that AtSWEET12 restricts sucrose availability in the apoplast, thereby limiting pathogen multiplication. Localization studies with GUS- and YFP-translational fusion lines indicate that during pathogen infection, sucrose efflux in the apoplast is regulated by an increased accumulation of AtSWEET12 at the plasma membrane, coupled with a concurrent reduction of AtSWEET11 protein. Our findings suggest that AtSWEET11 and AtSWEET12 interact, and post-translational modifications such as phosphorylation and heterooligomerization likely regulate their function in controlling apoplastic sucrose levels. In this study, we uncover a novel mechanism of pathogen starvation as a broad-spectrum disease resistance strategy in which plants modulate sucrose efflux via AtSWEET12 to combat foliar bacterial pathogens.