Concurrent activation of cell death-regulating signaling pathways by singlet oxygen in Arabidopsis thaliana

Authors

  • Antoine Danon,

    1. Institute of Plant Sciences, Plant Genetics, Swiss Federal Institute of Technology (ETH), CH - 8092 Zürich, Switzerland,
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    • Present address: Laboratoire Androgenèse et Biotechnologie, Université de Picardie Jules Verne, 33 rue Saint-Leu, 80039 Amiens Cedex 1, France.

  • Otto Miersch,

    1. Institute of Plant Biochemistry, Halle, Germany, and
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  • Georg Felix,

    1. Friedrich Miescher-Institute, Basel, Switzerland
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  • Roel G.L. op den Camp,

    1. Institute of Plant Sciences, Plant Genetics, Swiss Federal Institute of Technology (ETH), CH - 8092 Zürich, Switzerland,
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  • Klaus Apel

    Corresponding author
    1. Institute of Plant Sciences, Plant Genetics, Swiss Federal Institute of Technology (ETH), CH - 8092 Zürich, Switzerland,
      (fax +0041 1 632 1239; e-mail klaus.apel@ipw.biol.ethz.ch).
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(fax +0041 1 632 1239; e-mail klaus.apel@ipw.biol.ethz.ch).

Summary

Upon a dark/light shift the conditional flu mutant of Arabidopsis starts to generate singlet oxygen (1O2), a non-radical reactive oxygen species that is restricted to the plastid compartment. Immediately after the shift, plants stop growing and develop necrotic lesions. We have established a protoplast system, which allows detection and characterization of the death response in flu induced by the release of 1O2. Vitamin B6 that quenches 1O2 in fungi was able to protect flu protoplasts from cell death. Blocking ethylene production was sufficient to partially inhibit the death reaction. Similarly, flu mutant seedlings expressing transgenic NahG were partially protected from the death provoked by the release of 1O2, indicating a requirement for salicylic acid (SA) in this process, whereas in cells depleted of both, ethylene and SA, the extent of cell death was reduced to the wild-type level. The flu mutant was also crossed with the jasmonic acid (JA)-depleted mutant opr3, and with the JA, OPDA and dinor OPDA (dnOPDA)-depleted dde2-2 mutant. Analysis of the resulting double mutants revealed that in contrast to the JA-induced suppression of H2O2/superoxide-dependent cell death reported earlier, JA promotes singlet oxygen-mediated cell death in flu, whereas other oxylipins such as OPDA and dnOPDA antagonize this death-inducing activity of JA.

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