期刊
PLANT CELL AND ENVIRONMENT
卷 43, 期 6, 页码 1558-1570出版社
WILEY
DOI: 10.1111/pce.13753
关键词
Arabidopsis; botrytis; catabolism; defense; feedback; jasmonate; resistance; signalling; wounding
资金
- Agence Nationale de la Recherche [12-BSV8-005]
- Centre National de la Recherche Scientifique
- Ministere de l'Enseignement Superieur et de la Recherche Scientifique
- Schweizerischer Nationalfonds zur Forderung der Wissenschaftlichen Forschung [31003A_169278]
- Universite de Strasbourg [IdEx-2014-208e]
- Swiss National Science Foundation (SNF) [31003A_169278] Funding Source: Swiss National Science Foundation (SNF)
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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