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<dc:title xml:lang="fr">L'homéostasie catabolique des jasmonates et son impact sur la signalisation des réponses aux stress chez Arabidopsis thaliana</dc:title>
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<dc:subject xml:lang="fr">Jasmonates</dc:subject>
<dc:subject xml:lang="fr">Catabolisme</dc:subject>
<dc:subject xml:lang="fr">Signalisation basale</dc:subject>
<dc:subject xml:lang="fr">Jao</dc:subject>
<dc:subject xml:lang="fr">Feedback</dc:subject>
<dc:subject xml:lang="fr">Stress biotiques et abiotiques</dc:subject>
<dc:subject xml:lang="fr">Résistance</dc:subject>
<dc:subject xml:lang="en">Jasmonates</dc:subject>
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<tef:elementdEntree autoriteExterne="032353324" autoriteSource="Sudoc">Plantes -- Moyens de défense</tef:elementdEntree>
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<dcterms:abstract xml:lang="fr">Pour se défendre contre les herbivores ou les microorganismes nécrotrophes les plantes supérieures utilisent les jasmonates (JAs), en particulier l’hormone jasmonoyl-isoleucine (JA-Ile), pour activer la signalisation défensive. Les JAs régulent aussi des réponses contre des stress abiotiques. Mes travaux de thèse ont prouvé l’importance d’une signalisation JAs basale, et sa répression par trois oxydases d’acide jasmonique nommées JAO, dont l’action définit un mécanisme de détournement métabolique inédit. En aval de l'action du JA-Ile, deux voies cataboliques distinctes sont activées pour atténuer la signalisation induite. A l’aide de nouvelles lignées de plantes bloquées, pour l’une, l’autre ou les deux voies, mes recherches ont démontré leurs rôles respectifs dans l’élimination du JA-Ile en réponse à l’herbivorie ou à l’infection. Elles ont révélé qu’un catabolisme ralenti du JA-Ile limite sélectivement le gain en défense lorsque des régulateurs négatifs de la signalisation sont surstimulés. Nos résultats apportent de nouvelles connaissances sur les mécanismes cataboliques des JAs régulant les signalisations basales et induites.</dcterms:abstract>
<dcterms:abstract xml:lang="en">For defending against herbivores or necrotrophic microorganisms, higher plants rely on jasmonates (JAs), particularly on the hormone jasmonoyl-isoleucine (JA-Ile), to signal adaptive changes. JAs also modulate tolerance to abiotic stresses. My thesis work demonstrated the importance of basal JAs signalling, and its repression by three jasmonic acid oxidases called JAO, whose action defines a new metabolic diversion mechanism with regulatory properties. Using omics approaches, we defined the spectrum of responses activated in jao2 mutants. Downstream of JA-Ile action, two distinct catabolic pathways of JA-Ile are activated to attenuate induced signalling. Owing to the generation of new higher order mutant plant lines impaired in one, the other, or both pathways, my research demonstrated their respective roles in JA-Ile elimination in response to herbivory and infection. It particularly revealed that restrained JA-Ile catabolism results in increased defense only when negative regulators are not overstimulated. Our results provide new knowledge of JAs catabolic mechanisms regulating basal and induced signalling.</dcterms:abstract>
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