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A MYB Transcription Factor Regulates Very-Long-Chain Fatty Acid Biosynthesis for Activation of the Hypersensitive Cell Death Response in Arabidopsis^[W],[OA]

^a Laboratoire des Interactions Plantes-Microorganismes, Unité Mixte de Recherche 2594/441, 31320 Castanet-Tolosan cedex, France
^b Laboratoire de Biogenèse Membranaire, Unité Mixte de Recherche 5200, Université Victor Segalen Bordeaux 2, F-33000 Bordeaux cedex, France
^c Institute of Plant Biochemistry, Halle, D-06120 Germany
^d Laboratoire des Phytooxylipines, Institut de Biologie Moléculaire des Plantes, Unité Propre de Recherche 2357, 67083 Strasbourg Cedex, France

⁴ Address correspondence to 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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