CYP94-mediated jasmonoyl-isoleucine hormone oxidation shapes jasmonate profiles and attenuates defence responses to Botrytis cinerea infection

© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.

Bibliographische Detailangaben
Veröffentlicht in:Journal of experimental botany. - 1985. - 66(2015), 13 vom: 21. Juli, Seite 3879-92
1. Verfasser: Aubert, Yann (VerfasserIn)
Weitere Verfasser: Widemann, Emilie, Miesch, Laurence, Pinot, Franck, Heitz, Thierry
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2015
Zugriff auf das übergeordnete Werk:Journal of experimental botany
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Antifungal defence Arabidopsis cytochrome P450 hormone homeostasis jasmonate catabolism signalling. Arabidopsis Proteins Cyclopentanes mehr... Oxylipins jasmonoyl-isoleucine Isoleucine 04Y7590D77 jasmonic acid 6RI5N05OWW Cytochrome P-450 Enzyme System 9035-51-2 cytochrome P-450 94B3, Arabidopsis EC 1.- cytochrome P-450 94C1, Arabidopsis Salicylic Acid O414PZ4LPZ
Beschreibung
Zusammenfassung:© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.
Induced resistance to the necrotrophic pathogen Botrytis cinerea depends on jasmonate metabolism and signalling in Arabidopsis. We have presented here extensive jasmonate profiling in this pathosystem and investigated the impact of the recently reported jasmonoyl-isoleucine (JA-Ile) catabolic pathway mediated by cytochrome P450 (CYP94) enzymes. Using a series of mutant and overexpressing (OE) plant lines, we showed that CYP94B3 and CYP94C1 are integral components of the fungus-induced jasmonate metabolic pathway and control the abundance of oxidized conjugated but also some unconjugated derivatives, such as sulfated 12-HSO4-JA. Despite causing JA-Ile overaccumulation due to impaired oxidation, CYP94 deficiency had negligible impacts on resistance, associated with enhanced JAZ repressor transcript levels. In contrast, plants overexpressing (OE) CYP94B3 or CYP94C1 were enriched in 12-OH-JA-Ile or 12-COOH-JA-Ile respectively. This shift towards oxidized JA-Ile derivatives was concomitant with strongly impaired defence gene induction and reduced disease resistance. CYP94B3-OE, but unexpectedly not CYP94C1-OE, plants displayed reduced JA-Ile levels compared with the wild type, suggesting that increased susceptibility in CYP94C1-OE plants may result from changes in the hormone oxidation ratio rather than absolute changes in JA-Ile levels. Consistently, while feeding JA-Ile to seedlings triggered strong induction of JA pathway genes, induction was largely reduced or abolished after feeding with the CYP94 products 12-OH-JA-Ile and 12-COOH-JA-Ile, respectively. This trend paralleled in vitro pull-down assays where 12-COOH-JA-Ile was unable to promote COI1-JAZ9 co-receptor assembly. Our results highlight the dual function of CYP94B3/C1 in antimicrobial defence: by controlling hormone oxidation status for signal attenuation, these enzymes also define JA-Ile as a metabolic hub directing jasmonate profile complexity
Beschreibung:Date Completed 28.03.2016
Date Revised 13.11.2018
published: Print-Electronic
Citation Status MEDLINE
ISSN:1460-2431
DOI:10.1093/jxb/erv190