NH(4) (+) protects tomato plants against Pseudomonas syringae by activation of systemic acquired acclimation

NH(4) (+) nutrition provokes mild toxicity by enhancing H(2)O(2) accumulation, which acts as a signal activating systemic acquired acclimation (SAA). Until now, induced resistance mechanisms in response to an abiotic stimulus and related to SAA were only reported for exposure to a subsequent abiotic stress. Herein, the first evidence is provided that this acclimation to an abiotic stimulus induces resistance to later pathogen infection, since NH(4) (+) nutrition (N-NH(4) (+))-induced resistance (NH(4) (+)-IR) against Pseudomonas syringae pv tomato DC3000 (Pst) in tomato plants was demonstrated. N-NH(4) (+) plants displayed basal H(2)O(2), abscisic acid (ABA), and putrescine (Put) accumulation. H(2)O(2) accumulation acted as a signal to induce ABA-dependent signalling pathways required to prevent NH(4) (+) toxicity. This acclimatory event provoked an increase in resistance against later pathogen infection. N-NH(4) (+) plants displayed basal stomatal closure produced by H(2)O(2) derived from enhanced CuAO and rboh1 activity that may reduce the entry of bacteria into the mesophyll, diminishing the disease symptoms as well as strongly inducing the oxidative burst upon Pst infection, favouring NH(4) (+)-IR. Experiments with inhibitors of Put accumulation and the ABA-deficient mutant flacca demonstrated that Put and ABA downstream signalling pathways are required to complete NH(4) (+)-IR. The metabolic profile revealed that infected N-NH(4) (+) plants showed greater ferulic acid accumulation compared with control plants. Although classical salicylic acid (SA)-dependent responses against biotrophic pathogens were not found, the important role of Put in the resistance of tomato against Pst was demonstrated. Moreover, this work revealed the cross-talk between abiotic stress acclimation (NH(4) (+) nutrition) and resistance to subsequent Pst infection.