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Jasmonic Acid Signaling Modulates Ozone-Induced Hypersensitive Cell Death

Mulpuri V. Rao, Hyung-il Lee, Robert A. Creelman, John E. Mullet and Keith R. Davis
The Plant Cell
Vol. 12, No. 9 (Sep., 2000), pp. 1633-1646
DOI: 10.2307/3871179
Stable URL: http://www.jstor.org/stable/3871179
Page Count: 14
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Jasmonic Acid Signaling Modulates Ozone-Induced Hypersensitive Cell Death
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Abstract

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 ${\rm O}_{3}\text{-induced}\ {\rm H}_{2}{\rm O}_{2}$ 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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