Plant Cell Advance Online Publication
Published on March 7, 2008; 10.1105/tpc.107.054858
OPEN ACCESS ARTICLE
Received August 10, 2007
Returned for revision November 30, 2007
Accepted February 20, 2008
A MYB Transcription Factor Regulates Very-Long-Chain Fatty Acid Biosynthesis for Activation of the Hypersensitive Cell Death Response in Arabidopsis
Sylvain Raffaele 1, Fabienne Vailleau 1, Amandine Léger 1, Jérôme Joubès 2, Otto Miersch 3, Carine Huard 1, Elisabeth Blée 4, Sébastien Mongrand 2, Frédéric Domergue 2, and Dominique Roby 1*
1 Laboratoire des Interactions Plantes-Microorganismes, Unité Mixte de Recherche 2594/441, 31320 Castanet-Tolosan cedex, France
2 Laboratoire de Biogenèse Membranaire, Unité Mixte de Recherche 5200, Université Victor Segalen Bordeaux 2, F-33000 Bordeaux cedex, France
3 Institute of Plant Biochemistry, Halle, D-06120 Germany
4 Laboratoire des Phytooxylipines, Institut de Biologie Moléculaire des Plantes, Unité Propre de Recherche 2357, 67083 Strasbourg Cedex, France
* To whom correspondence should be addressed. E-mail: roby{at}toulouse.inra.fr.
Plant immune responses to pathogen attack include the hypersensitive response (HR), a form of programmed cell death occurring at invasion sites. We previously reported on Arabidopsis thaliana MYB30, a transcription factor that acts as a positive regulator of a cell death pathway conditioning the HR. Here, we show by microarray analyses of Arabidopsis plants misexpressing MYB30 that the genes encoding the four enzymes forming the acyl-coA elongase complex are putative MYB30 targets. The acyl-coA elongase complex synthesizes very-long-chain fatty acids (VLCFAs), and the accumulation of extracellular VLCFA-derived metabolites (leaf epidermal wax components) was affected in MYB30 knockout mutant and overexpressing lines. In the same lines, a lipid extraction procedure allowing high recovery of sphingolipids revealed changes in VLCFA contents that were amplified in response to inoculation. Finally, the exacerbated HR phenotype of MYB30-overexpressing lines was altered by the loss of function of the acyl-ACP thioesterase FATB, which causes severe defects in the supply of fatty acids for VLCFA biosynthesis. Based on these findings, we propose a model in which MYB30 modulates HR via VLCFAs by themselves, or VLCFA derivatives, as cell death messengers in plants.
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