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Transgenic tobacco with a reduced catalase activity develops necrotic lesions and induces pathogenesis-related expression under high light

Authors

  • Sangpen Chamnongpol,

    1. Laboratorium voor Genetica, Department of Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), Universiteit Gent, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium
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    • Both authors have contributed equally to this work.

  • Hilde Willekens,

    1. Laboratorium voor Genetica, Department of Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), Universiteit Gent, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium
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    • Both authors have contributed equally to this work.

  • Christian Langebartels,

    1. Institut für Biochemische Pflanzenpathologie, GSF-Forschungszentrum für Umwelt und Gesundheit, D-85764 Oberschleißheim, Germany
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  • Marc Van Montagu,

    Corresponding author
    1. Laboratorium voor Genetica, Department of Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), Universiteit Gent, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium
      *For correspondence (fax +32 9 2645349).
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  • Dirk Inzé,

    1. Laboratoire Associé de l’Institut National de la Recherche Agronomique (France), Universiteit Gent, B-9000 Gent, Belgium
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  • Wim Van Camp

    1. Laboratorium voor Genetica, Department of Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), Universiteit Gent, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium
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*For correspondence (fax +32 9 2645349).

Abstract

Transgenic tobacco deficient in either Cat1 (Cat1AS), Cat2 (Cat2AS), or both (CatGH) was generated through sense and antisense technology. Cat1AS, Cat2AS, and CatGH plants showed no visible phenotype when grown at low light (100 µmol m−2 sec−1. Under these conditions, deficiency in Cat1 and/or Cat2 did not lead to constitutive pathogenesis-related (PR-1) expression and did not potentiate PR-1 induction by exogenous salicylic acid. This demonstrates that catalase suppression per se is not a sufficient signal for PR-1 induction. In Cat1-deficient plants exposed to higher light intensities (250–1000 µmol m−2 sec−1), PR-1 expression was induced without pathogenic challenge and multiplication of Pseudomonas syringae pv. syringae was repressed. Yet, it is unlikely that Cat1 deficiency is mimicking the mode of action of salicylic acid in tobacco, because, concurrent with PR-1 induction, Cat1 deficiency at high light provoked severe leaf damage, characterized by white necrotic lesions. Taken together, these results do not support the model that catalase inactivation is the key route by which salicylic acid induces PR defense responses in healthy tissue. However, because catalase deficiency is potentially lethal to leaves, catalase inactivation by salicylic acid could be of importance in the establishment of hypersensitive responses.

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