Flg22 regulates the release of an ethylene response factor substrate from MAP kinase 6 in Arabidopsis thaliana via ethylene signaling

• Published in: Proceedings of the National Academy of Sciences - PNAS 2009-05, Vol.106 (19), p.8067-8072
• Main Authors: Bethke, Gerit, Unthan, Tino, Uhrig, Joachim F, Pöschl, Yvonne, Gust, Andrea A, Scheel, Dierk, Lee, Justin
• Format: Article
• Language: English
• Subjects: Arabidopsis - enzymology; Arabidopsis Proteins - physiology; Arabidopsis thaliana; Bacteria; bacterial diseases of plants; bacterial proteins; Biological Sciences; Biosynthesis; Bleaching; Botrytis cinerea; Data processing; Enzymes; Ethylene; ethylene response factor; Ethylenes - chemistry; Flagellin - metabolism; flagellum; flg22 protein; Flowers & plants; Fluorescence Resonance Energy Transfer; fungal diseases of plants; gene expression; Gene Expression Profiling; Gene expression regulation; Gene Expression Regulation, Plant; Genes; Genes, Plant; Genetic Techniques; Immunity; Kinases; MAP kinase; messenger RNA; microarray technology; mitogen-activated protein kinase; Mitogen-Activated Protein Kinase 6 - metabolism; Models, Biological; Mutation; Oligonucleotide Array Sequence Analysis; Pathogens; peptides; Phosphorylation; Plant cells; Plants; promoter regions; Promoters; protein phosphorylation; protein-protein interactions; Proteins; Protoplasts; Pseudomonas syringae pv. phaseolicola; Signal Transduction; Stress; Substrates; Transcription factors; Transcriptional Activation
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.0810206106

Mitogen-activated protein kinase (MAPK)-mediated responses are in part regulated by the repertoire of MAPK substrates, which is still poorly elucidated in plants. Here, the in vivo enzyme-substrate interaction of the Arabidopsis thaliana MAP kinase, MPK6, with an ethylene response factor (ERF104) is shown by fluorescence resonance energy transfer. The interaction was rapidly lost in response to flagellin-derived flg22 peptide. This complex disruption requires not only MPK6 activity, which also affects ERF104 stability via phosphorylation, but also ethylene signaling. The latter points to a novel role of ethylene in substrate release, presumably allowing the liberated ERF104 to access target genes. Microarray data show enrichment of GCC motifs in the promoters of ERF104-up-regulated genes, many of which are stress related. ERF104 is a vital regulator of basal immunity, as altered expression in both erf104 and overexpressors led to more growth inhibition by flg22 and enhanced susceptibility to a non-adapted bacterial pathogen.