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Plant Cell, Vol. 12, 1633-1646, September 2000, Copyright © 2000, American Society of Plant Physiologists

Jasmonic Acid Signaling Modulates Ozone-Induced Hypersensitive Cell Death

Mulpuri V. Raoa, Hyung-il Leeb, Robert A. Creelmanc, John E. Mulletc, and Keith R. Davisd
a Plant Biotechnology Center, Ohio State University, Columbus, Ohio 43210
b Biotechnology Center, Cook College–Foran Hall, Rutgers University, New Brunswick, New Jersey 08901
c Crop Biotechnology Center, Department of Biophysics and Biochemistry, Texas A & M University, College Station, Texas 77843
d Paradigm Genetics, Inc., 104 Alexander Drive, Research Triangle Park, North Carolina 27709

Correspondence to: Keith R. Davis, kdavis{at}paragen.com (E-mail), 919-572-6764 (fax)

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 (O3) 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 O3-induced cell death. Expression of salicylate hydroxylase (NahG) in Cvi-0 reduced O3-induced cell death. Methyl jasmonate (Me-JA) pretreatment of Cvi-0 decreased O3-induced H2O2 content and SA concentrations and completely abolished O3-induced cell death. Cvi-0 synthesized as much JA as did Col-0 in response to O3 exposure but exhibited much less sensitivity to exogenous Me-JA. Analyses of the responses to O3 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 O3-induced HR-like cell death.




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