Stress- and pathway-specific impacts of impaired jasmonoyl-isoleucine (JA-Ile) catabolism on defense signalling and biotic stress resistance.
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Marquis V
Institut de Biologie Moléculaire des Plantes (IBMP) du CNRS, Université de Strasbourg, Strasbourg, France.
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Smirnova E
Institut de Biologie Moléculaire des Plantes (IBMP) du CNRS, Université de Strasbourg, Strasbourg, France.
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Poirier L
Institut de Biologie Moléculaire des Plantes (IBMP) du CNRS, Université de Strasbourg, Strasbourg, France.
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Zumsteg J
Institut de Biologie Moléculaire des Plantes (IBMP) du CNRS, Université de Strasbourg, Strasbourg, France.
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Schweizer F
Department of Plant Molecular Biology, University of Lausanne, Lausanne, Switzerland.
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Reymond P
Department of Plant Molecular Biology, University of Lausanne, Lausanne, Switzerland.
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Heitz T
Institut de Biologie Moléculaire des Plantes (IBMP) du CNRS, Université de Strasbourg, Strasbourg, France.
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Published in:
- Plant, cell & environment. - 2020
English
Jasmonate synthesis and signalling are essential for plant defense upregulation upon herbivore or microbial attacks. Stress-induced accumulation of jasmonoyl-isoleucine (JA-Ile), the bioactive hormonal form triggering transcriptional changes, is dynamic and transient because of the existence of potent removal mechanisms. Two JA-Ile turnover pathways operate in Arabidopsis, consisting in cytochrome P450 (CYP94)-mediated oxidation and deconjugation by the amidohydrolases IAR3/ILL6. Understanding their impacts was previously blurred by gene redundancy and compensation mechanisms. Here we address the consequences of blocking these pathways on jasmonate homeostasis and defenses in double-2ah, triple-3cyp mutants, and a quintuple-5ko line deficient in all known JA-Ile-degrading activities. These lines reacted differently to either mechanical wounding/insect attack or fungal infection. Both pathways contributed additively to JA-Ile removal upon wounding, but their impairement had opposite impacts on insect larvae feeding. By contrast, only the ah pathway was essential for JA-Ile turnover upon infection by Botrytis, yet only 3cyp was more fungus-resistant. Despite building-up extreme JA-Ile levels, 5ko displayed near-wild-type resistance in both bioassays. Molecular analysis indicated that restrained JA-Ile catabolism resulted in enhanced defense/resistance only when genes encoding negative regulators were not simultaneously overstimulated. This occurred in discrete stress- and pathway-specific combinations, providing a framework for future defense-enhancing strategies.
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Open access status
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green
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Persistent URL
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https://sonar.ch/global/documents/186316
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