The common bean rust fungus reduces harvests of the dry, edible common bean. Natural resistance genes in the plant can provide protection until a fungal strain that breaks resistance emerges. In this study, we demonstrate that benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester (BTH) sprayed on susceptible beans induces resistance to common bean rust. Protection occurred as soon as 72 h after treatment and resulted in no signs of disease 10 days after inoculation with rust spores. By contrast, the susceptible control plants sustained heavy infections and died. To understand the effect BTH has on the bean proteome, we measured the changes of accumulation for 3,973 proteins using mass spectrometry. The set of 409 proteins with significantly increased accumulation in BTH-treated leaves included receptor-like kinases SOBIR1, CERK1, and LYK5, which perceive pathogens, and EDS1, a regulator of the salicylic acid defense pathway. Other proteins that likely contributed to resistance included pathogenesis-related proteins, a full complement of enzymes that catalyze phenylpropanoid biosynthesis, and protein receptors, transporters, and enzymes that modulate other defense responses controlled by jasmonic acid, ethylene, brassinosteroid, abscisic acid, and auxin. Increases in the accumulation of proteins required for vesicle-mediated protein secretion and RNA splicing occurred as well. By contrast, more than half of the 168 decreases belonged to chloroplast proteins and proteins involved in cell expansion. These results reveal a set of proteins needed for rust resistance and reaffirm the utility of BTH to control disease by amplifying the natural immune system of the bean plant.
Keywords: BTH; Phaseolus vulgaris; Uromyces appendiculatus; bean rust; mass spectrometry; proteomics; systemic acquired resistance.