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在拟南芥中,鞭毛蛋白22(Flg22)通过乙烯信号传导调节乙烯反应因子底物从促分裂原活化蛋白激酶6(MAP激酶6)的释放。

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

作者信息

Bethke Gerit, Unthan Tino, Uhrig Joachim F, Pöschl Yvonne, Gust Andrea A, Scheel Dierk, Lee Justin

机构信息

Leibniz Institute of Plant Biochemistry, Weinberg 3, D-06120, Halle, Germany.

出版信息

Proc Natl Acad Sci U S A. 2009 May 12;106(19):8067-72. doi: 10.1073/pnas.0810206106. Epub 2009 Apr 29.

Abstract

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.

摘要

丝裂原活化蛋白激酶(MAPK)介导的反应部分受MAPK底物库的调节,而植物中MAPK底物库仍未得到充分阐明。在此,通过荧光共振能量转移展示了拟南芥MAP激酶MPK6与乙烯反应因子(ERF104)在体内的酶-底物相互作用。该相互作用在响应鞭毛蛋白衍生的flg22肽时迅速丧失。这种复合物的破坏不仅需要MPK6的活性,MPK6的活性还通过磷酸化影响ERF104的稳定性,而且还需要乙烯信号传导。后者表明乙烯在底物释放中具有新作用,推测这使得游离的ERF104能够作用于靶基因。微阵列数据显示,ERF104上调基因的启动子中GCC基序富集,其中许多基因与胁迫相关。ERF104是基础免疫的重要调节因子,因为在erf104和过表达植株中表达的改变导致flg22对生长的抑制作用更强,并且对非适应性细菌病原体的易感性增强。

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