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 hypersensitiveresponse (HR), a form of programmed cell death occurring atinvasion sites. We previously reported on Arabidopsis thalianaMYB30, a transcription factor that acts as a positive regulatorof a cell death pathway conditioning the HR. Here, we show bymicroarray analyses of Arabidopsis plants misexpressing MYB30that the genes encoding the four enzymes forming the acyl-coAelongase complex are putative MYB30 targets. The acyl-coA elongasecomplex synthesizes very-long-chain fatty acids (VLCFAs), andthe accumulation of extracellular VLCFA-derived metabolites(leaf epidermal wax components) was affected in MYB30 knockoutmutant and overexpressing lines. In the same lines, a lipidextraction procedure allowing high recovery of sphingolipidsrevealed changes in VLCFA contents that were amplified in responseto inoculation. Finally, the exacerbated HR phenotype of MYB30-overexpressinglines was altered by the loss of function of the acyl-ACP thioesteraseFATB, which causes severe defects in the supply of fatty acidsfor VLCFA biosynthesis. Based on these findings, we proposea model in which MYB30 modulates HR via VLCFAs by themselves,or VLCFA derivatives, as cell death messengers in plants.