The outcomes of concentration-specific interactions between salicylate and jasmonate signaling include synergy, antagonism, and oxidative stress leading to cell death

Salicylic acid ( SA) has been proposed to antagonize jasmonic acid ( JA) biosynthesis and signaling. We report, however, that in salicylate hydroxylase- expressing tobacco ( Nicotiana tabacum) plants, where SA levels were reduced, JA levels were not elevated during a hypersensitive response elicited by Pseudomonas syringae pv phaseolicola. The effects of cotreatment with various concentrations of SA and JA were assessed in tobacco and Arabidopsis ( Arabidopsis thaliana). These suggested that there was a transient synergistic enhancement in the expression of genes associated with either JA ( PDF1.2 [ defensin] and Thi1.2 [ thionin]) or SA ( PR1 [ PR1a- beta- glucuronidase in tobacco]) signaling when both signals were applied at low ( typically 10 100 mu M) concentrations. Antagonism was observed at more prolonged treatment times or at higher concentrations. Similar results were also observed when adding the JA precursor, alpha- linolenic acid with SA. Synergic effects on gene expression and plant stress were NPR1- and COI1- dependent, SA- and JA- signaling components, respectively. Electrolyte leakage and Evans blue staining indicated that application of higher concentrations of SA + JA induced plant stress or death and elicited the generation of apoplastic reactive oxygen species. This was indicated by enhancement of hydrogen peroxide- responsive AoPR10-beta-glucuronidase expression, suppression of plant stress/death using catalase, and direct hydrogen peroxide measurements. Our data suggests that the outcomes of JA- SA interactions could be tailored to pathogen/pest attack by the relative concentration of each hormone.