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Redox Regulation by Thioredoxins in Plant Immunity /


Members of Arabidopsis thaliana cytosolic thioredoxins play various roles in plant defense against pathogen infections. Thioredoxin h5 (AtTRXh5) catalyzes the reduction and activation of NPR1, a master regulator of plant systemic acquired resistance (SAR) to various pathogens. Thioredoxin h3 (AtTRXh3) and AtTRXh5 confer plant's sensitivity to victorin, which is an effector secreted by Cochliobolus victoriae to establish pathogenesis. To extend the analysis of the roles of AtTRXh3 and AtTRXh5 in defense against both biotrophic and necrotrophic pathogens, we challenged mutant trxs to Pseudomonas syringae and Botrytis cinerea infections. We show that although AtTRXh5 is known to catalyze the NPR1 oligomer-to-monomer switch, it is not required for induced resistance (IR) against a biotrophic pathogen. Furthermore, our bioassay results suggest that reduction of NPR1 by AtTRXh5 may be replaced by other thioredoxins in the cytosol, thus enabling plants to mount IR even in the absence of both AtTRXh3 and AtTRXh5. We also found that AtTRXh3 and AtTRXh5 are required for full immunity against Botrytis cinerea, a necrotrophic pathogen. Quantitative proteomic approach using isotope coded affinity tag (ICAT) -labeling was utilized to grasp how Arabidopsis redoxome alters upon defense elicitation by benzo(1,2,3)thiadiazole -7-carbothioic acid (BTH), a potent analog of salicylic acid. Our analysis suggests that TRXs may inhibit defense- induced redox alterations of proteins, many of which have implications in both salicylic acid and jasmonic acid- mediated defense pathways

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