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J. Biol. Chem., Vol. 280, Issue 13, 12168-12180, April 1, 2005

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The Mitochondrial Type II Peroxiredoxin F Is Essential for Redox Homeostasis and Root Growth of Arabidopsis thaliana under Stress^*

Iris Finkemeier, Megan Goodman, Petra Lamkemeyer, Andrea Kandlbinder, Lee J. Sweetlove¶, and Karl-Josef Dietz||

From the Department of Plant Physiology and Biochemistry, University of Bielefeld, 33501 Bielefeld, Germany and the Department of Plant Sciences, University of Oxford, South Parks Road, Oxford OX1 3RP, United Kingdom

Peroxiredoxins (Prx) have recently moved into the focus of plant and animal research in the context of development, adaptation, and disease, as they function both in antioxidant defense by reducing a broad range of toxic peroxides and in redox signaling relating to the adjustment of cell redox and antioxidant metabolism. At-PrxII F is one of six type II Prx identified in the genome of Arabidopsis thaliana and the only Prx that is targeted to the plant mitochondrion. Therefore, it might be assumed to have functions similar to the human 2-Cys Prx (PRDX3) and type II Prx (PRDX5) and yeast 1-Cys Prx that likewise have mitochondrial localizations. This paper presents a characterization of PrxII F at the level of subcellular distribution, activity, and reductive regeneration by mitochondrial thioredoxin and glutaredoxin. By employing tDNA insertion mutants of A. thaliana lacking expression of AtprxII F (KO-AtPrxII F), it is shown that under optimal environmental conditions the absence of PrxII F is almost fully compensated for, possibly by increases in activity of mitochondrial ascorbate peroxidase and glutathione-dependent peroxidase. However, a stronger inhibition of root growth in KO-AtPrxII F seedlings as compared with wild type is observed under stress conditions induced by CdCl₂ as well as after administration of salicylhydroxamic acid, an inhibitor of cyanide-insensitive respiration. Simultaneously, major changes in the abundance of both nuclear and mitochondria-encoded transcripts were observed. These results assign a principal role to PrxII F in antioxidant defense and possibly redox signaling in plants cells.

Received for publication, November 22, 2004 , and in revised form, December 21, 2004.

^* This work was supported in part by the Deutsche Forschungsgemeinschaft within the Special Research Focus FOR 387 (TP 3, Redox Regulation of Nuclear Gene Expression) and Di 346/6 (Organellar Prx). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ Supported by a David Phillips Research Fellowship from the Biotechnology and Biological Sciences Research Council, UK.

^|| To whom correspondence should be addressed: Dept. of Plant Physiology and Biochemistry/W5, University of Bielefeld, 33501 Bielefeld, Germany. Tel.: 49-521-106-5589; Fax: 49-521-106-6039; E-mail: karl-josef.dietz{at}uni-bielefeld.de.

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