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| Standard Gene Set Name | RAFFAELE_WT-INDUCED_MYB30OX/WT-UP_MYB30AS/WT_DN |
| Species | Arabidopsis thaliana |
| Brief Description | Induced in the wild-type, up-regulated in MYB30ox compared to wild-type, and repressed in MYB30as compared to wild-type (upon inoculation with Xcc147) (Table S2 PubmedID:18326828) |
| Full Description/Abstract | 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 |
| External Pathway ID/Pubmed ID | 18326828 |
| Source | Literature |
| Contributor/Author | Liming Lai and Xijin Ge |
| Organization of contributer | South Dakota State University |
| External URL | http://www.plantcell.org/cgi/reprint/20/3/752 |