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

被引:295
作者
Bethke, Gerit [1 ]
Unthan, Tino [1 ]
Uhrig, Joachim F. [2 ]
Poeschl, Yvonne [1 ]
Gust, Andrea A. [3 ]
Scheel, Dierk [1 ]
Lee, Justin [1 ]
机构
[1] Leibniz Inst Plant Biochem, D-06120 Halle, Germany
[2] Univ Cologne, Bot Inst 3, D-50931 Cologne, Germany
[3] Univ Tubingen, Ctr Plant Mol Biol, D-72076 Tubingen, Germany
关键词
defense; elicitor; FRET; signal transduction; ACTIVATED PROTEIN-KINASES; TRANSCRIPTION FACTOR; GENE-EXPRESSION; MPK4; ACTIVATION; SALICYLIC-ACID; CELL-DEATH; STRESS; PATHWAYS; CASCADE; DOMAIN;
D O I
10.1073/pnas.0810206106
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:8067 / 8072
页数:6
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