Reactive oxygen species dosage in Arabidopsis chloroplasts can improve resistance towards Colletotrichum higginsianum by the induction of WRKY33
• Arabidopsis plants overexpressing glycolate oxidase in chloroplasts (GO5) and loss-of-function mutants of the major peroxisomal catalase isoform, cat2-2, produce increased hydrogen peroxide (H₂O₂) amounts from the respective organelles when subjected to photorespiratory conditions like increased l...
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Veröffentlicht in: | The New phytologist 2020-04, Vol.226 (1), p.189-204 |
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Sprache: | eng |
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Zusammenfassung: | • Arabidopsis plants overexpressing glycolate oxidase in chloroplasts (GO5) and loss-of-function mutants of the major peroxisomal catalase isoform, cat2-2, produce increased hydrogen peroxide (H₂O₂) amounts from the respective organelles when subjected to photorespiratory conditions like increased light intensity.
• Here, we have investigated if and how the signaling processes triggered by H₂O₂ production in response to shifts in environmental conditions and the concomitant induction of indole phytoalexin biosynthesis in GO5 affect susceptibility towards the hemibiotrophic fungus Colletotrichum higginsianum.
• Combining histological, biochemical, and molecular assays, we found that the accumulation of the phytoalexin camalexin was comparable between GO genotypes and cat2-2 in the absence of pathogen. Compared with wild-type, GO5 showed improved resistance after light-shift-mediated production of H₂O₂, whereas cat2-2 became more susceptible and allowed significantly more pathogen entry. Unlike GO5, cat2-2 suffered from severe oxidative stress after light shifts, as indicated by glutathione pool size and oxidation state.
• We discuss a connection between elevated oxidative stress and dampened induction of salicylic acid mediated defense in cat2-2. Genetic analyses demonstrated that induced resistance of GO5 is dependent on WRKY33, but not on camalexin production. We propose that indole carbonyl nitriles might play a role in defense against C. higginsianum. |
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ISSN: | 0028-646X 1469-8137 |
DOI: | 10.1111/nph.16332 |