MYB Transcription Factor Regulates Very-Long-Chain Fatty Acid Biosynthesis for Activation of the Hypersensitive Cell Death Response in Arabidopsis

• Published in: The Plant cell Vol. 20; no. 3; pp. 752 - 767
• Main Authors: Raffaele, Sylvain, Vailleau, Fabienne, Léger, Amandine, Joubès, Jérôme, Miersch, Otto, Huard, Carine, Blée, Elisabeth, Mongrand, Sébastien, Domergue, Frédéric, Roby, Dominique
• Format: Journal Article
• Language: English
• Published: United States American Society of Plant Biologists 01.03.2008; American Society of Plant Biologists (ASPB)
• Subjects: Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis Proteins - physiology; Arabidopsis thaliana; Biosynthesis; Cell death; Cell Death - genetics; Cellular Biology; Fatty acids; Fatty Acids - biosynthesis; Gene Expression Regulation, Plant; Genes; Inoculation; Life Sciences; Lipids; Models, Biological; Oligonucleotide Array Sequence Analysis; Pathogens; Phenotypes; Plant cells; Plants, Genetically Modified; Reverse Transcriptase Polymerase Chain Reaction; Transcription Factors - genetics; Transcription Factors - metabolism; Transcription Factors - physiology; Waxes
• ISSN: 1040-4651; 1532-298X; 1532-298X
• DOI: 10.1105/tpc.107.054858

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.