title: The outcomes of concentration-specific interactions between salicylate and jasmonate signaling include synergy, antagonism, and oxidative stress leading to cell death.
abstract: 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 microm) 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.
authors.affiliation: Institute of Biological Science, University of Wales, Aberystwyth, United Kingdom. lum@aber.ac.uk
authors.forename: Luis A J
authors.initials: LA
authors.lastname: Mur
authors.forename: Paul
authors.initials: P
authors.lastname: Kenton
authors.forename: Rainer
authors.initials: R
authors.lastname: Atzorn
authors.forename: Otto
authors.initials: O
authors.lastname: Miersch
authors.forename: Claus
authors.initials: C
authors.lastname: Wasternack
mesh_terms: D017209:Apoptosis; D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism; D003517:Cyclopentanes / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D018506:Gene Expression Regulation, Plant; D006861:Hydrogen Peroxide / Q000378:metabolism; D006899:Mixed Function Oxygenases / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress; D054883:Oxylipins; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism; D030821:Plants, Genetically Modified / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D044224:Pseudomonas syringae / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D020156:Salicylic Acid / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology*; D015398:Signal Transduction; D014026:Nicotiana / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*
chemical_list: D029681:Arabidopsis Proteins; D003517:Cyclopentanes; D054883:Oxylipins; D010940:Plant Proteins; D017382:Reactive Oxygen Species; C011006:jasmonic acid; D006861:Hydrogen Peroxide; D006899:Mixed Function Oxygenases; C022619:salicylate 1-monooxygenase; D020156:Salicylic Acid