Jasmonic acid signaling modulates ozone-induced hypersensitive cell death

Recent studies suggest that cross-talk between salicylic acid (SA)-, jasmonic acid (JA)-, and ethylene-dependent signaling pathways regulates plant responses to both abiotic and biotic stress factors. Earlier studies demonstrated that ozone (O-3) exposure activates a hypersensitive response (HR)-like cell death pathway in the Arabidopsis ecotype Cvi-0. We now have confirmed the role of SA and JA signaling in influencing O-3-induced cell death. Expression of salicylate hydroxylase (NahG) in Cvi-0 reduced O-3-induced cell death. Methyl jasmonate (Me-JA) pretreatment of Cvi-O decreased O-3-induced H2O2 content and SA concentrations and completely abolished O-3-induced cell death. Cvi-0 synthesized as much JA as did Col-0 in response to O-3 exposure but exhibited much less sensitivity to exogenous Me-JA. Analyses of the responses to O-3 Of the JA-signaling mutants jar1 and fad3/7/8 also demonstrated an antagonistic relationship between JA- and SA-signaling pathways in controlling the magnitude of O-3-induced HR-like cell death.