Changes in hydrogen peroxide homeostasis trigger an active cell death process in tobacco

Authors

  • James F. Dat,

    1. Department of Plant Systems Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium,
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    • Present address: Laboratoire de Biologie et Ecophysiologie EA 3184, Université de Franche-Comté-INRA, F-25030 Besançon Cedex, France.

  • Riikka Pellinen,

    1. Institute for Biotechnology, University of Helsinki, POB 56, Viikinkaari 5D, FIN-00014 Helsinki, Finland, and
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    • Present address: A.I. Virtanen Institute, University of Kuopio, POB 1627, FIN-70211 Kuopio, Finland.

  • Tom Beeckman,

    1. Department of Plant Systems Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium,
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  • Brigitte Van De Cotte,

    1. Department of Plant Systems Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium,
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  • Christian Langebartels,

    1. Institute of Biochemical Plant Pathology, GSF National Research Center for Environment and Health, Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany
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  • Jaakko Kangasjärvi,

    1. Institute for Biotechnology, University of Helsinki, POB 56, Viikinkaari 5D, FIN-00014 Helsinki, Finland, and
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  • Dirk Inzé,

    Corresponding author
    1. Department of Plant Systems Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium,
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  • Frank Van Breusegem

    1. Department of Plant Systems Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium,
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For correspondence (fax +32 9 264 5349; e-mail dirk.inze@gengenp.rug.ac.be).

Summary

In transgenic tobacco plants with reduced catalase activity, high levels of hydrogen peroxide (H2O2) can accumulate under photorespiratory conditions. Such a perturbation in H2O2 homeostasis induced cell death in clusters of palisade parenchyma cells, primarily along the veins. Ultrastructural alterations, such as chromatin condensation and disruption of mitochondrial integrity, took place before cell death. Furthermore, enhanced transcript levels of mitochondrial defense genes accompanied these mitochondrial changes. Pharmacological data indicated that the initiation and execution of cell death require de novo protein synthesis and that the signal transduction pathway leading to cell death involved changes in ion homeostasis, (de)phosphorylation events and an oxidative burst, as observed during hypersensitive responses. This oxidase-dependent oxidative burst is essential for cell death, but it is not required for the accumulation of defense proteins, suggesting a more prominent role for the oxidative burst in abiotic stress-induced cell death.

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