Titre
Reactive electrophile species activate defense gene expression in Arabidopsis.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Alméras, E.
Auteure/Auteur
Stolz, S.
Auteure/Auteur
Vollenweider, S.
Auteure/Auteur
Reymond, P.
Auteure/Auteur
Mène-Saffrané, L.
Auteure/Auteur
Farmer, E.E.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0960-7412
Statut éditorial
Publié
Date de publication
2003
Volume
34
Numéro
2
Première page
205
Dernière page/numéro d’article
216
Langue
anglais
Résumé
Compounds containing alpha,beta-unsaturated carbonyl groups are increasingly implicated as potent regulators of gene expression; some are powerful cytotoxins known to accumulate at the site of lesion formation in host-pathogen interactions. We used a robust measurement of photosynthetic efficiency to quantify the toxicity of a variety of lipid derivatives in Arabidopsis leaves. Small alpha,beta-unsaturated carbonyl compounds (e.g. acrolein and methyl vinyl ketone) were highly active and proved to be potent stimulators of expression of the pathogenesis-related gene HEL (PR4). These small volatile electrophiles were far more active than larger alkenal homologs like 2(E)-hexenal, and activated HEL expression in a manner independent of salicylate, ethylene, and jasmonate production/perception. Electrophile treatment massively increased the levels of unesterified cyclopentenone jasmonates, which themselves are electrophiles. Patterns of gene expression in response to electrophile treatment and in response to avirulent bacteria were compared, which revealed strikingly similar transcript profiles. The results broaden the range of known biologic effects of reactive electrophile species to include the activation of a pathogenesis-related gene (HEL) and genes involved in metabolism. Electrophiles can act as mediators of both genetic and biochemical effects on core defense signal transduction.
Sujets
PID Serval
serval:BIB_AD4336CAEF81
PMID
Open Access
Oui
Date de création
2008-01-24T19:05:37.611Z
Date de création dans IRIS
2025-05-21T03:56:36Z