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First published online August 25, 2006; 10.1104/pp.106.085472

Plant Physiology 142:595-608 (2006)
© 2006 American Society of Plant Biologists

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Right arrow Reactive Oxygen Species
ENVIRONMENTAL STRESS AND ADAPTATION TO STRESS

Interaction between Nitric Oxide and Ethylene in the Induction of Alternative Oxidase in Ozone-Treated Tobacco Plants1,[W]

Luisa Ederli, Roberta Morettini, Andrea Borgogni, Claus Wasternack, Otto Miersch, Lara Reale, Francesco Ferranti, Nicola Tosti2 and Stefania Pasqualini*

Department of Plant Biology and Agro-Environmental and Animal Biotechnology, University of Perugia, I–06121 Perugia, Italy (L.E., R.M., A.B., L.R., F.F., S.P.); Leibniz-Institut für Pflanzenbiochemie, D–06120 Halle (Saale), Germany (C.W., O.M.); and Institute of Plant Genetics, Consiglio Nazionale delle Ricerche, I–06128, Perugia, Italy (N.T.)

The higher plant mitochondrial electron transport chain contains, in addition to the cytochrome chain, an alternative pathway that terminates with a single homodimeric protein, the alternative oxidase (AOX). We recorded temporary inhibition of cytochrome capacity respiration and activation of AOX pathway capacity in tobacco plants (Nicotiana tabacum L. cv BelW3) fumigated with ozone (O3). The AOX1a gene was used as a molecular probe to investigate its regulation by signal molecules such as hydrogen peroxide, nitric oxide (NO), ethylene (ET), salicylic acid, and jasmonic acid (JA), all of them reported to be involved in the O3 response. Fumigation leads to accumulation of hydrogen peroxide in mitochondria and early accumulation of NO in leaf tissues. Although ET accumulation was high in leaf tissues 5 h after the start of O3 fumigation, it declined during the recovery period. There were no differences in the JA and 12-oxo-phytodienoic acid levels of treated and untreated plants. NO, JA, and ET induced AOX1a mRNA accumulation. Using pharmacological inhibition of ET and NO, we demonstrate that both NO- and ET-dependent pathways are required for O3-induced up-regulation of AOX1a. However, only NO is indispensable for the activation of AOX1a gene expression.


1 This work was supported by a grant from MIUR (National Project; COFIN 2005) and by a grant of Fondazione Cassa di Risparmio.

2 Present address: &LAB Srl, Via Strozzacapponi, 89/a, I–06071 Perugia, Italy.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Stefania Pasqualini (spas{at}unipg.it).

[W] The online version of this article contains Web-only data.

www.plantphysiol.org/cgi/doi/10.1104/pp.106.085472

* Corresponding author; e-mail spas{at}unipg.it; fax 39–0755856404.

Received June 20, 2006; accepted August 11, 2006; published August 25, 2006.




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