Arabidopsis MYB30 is a direct target of BES1 and cooperates with BES1 to regulate brassinosteroid-induced gene expression.
Arabidopsis MYB30 is a direct target of BES1 and cooperates with BES1 to regulate brassinosteroid-induced gene expression.
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DOI：
10.1111/j.1365-313x.2008.03778.x
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发表时间：
2009-04
期刊：
影响因子：
--
通讯作者：
Yin Y
中科院分区：
文献类型：
--
作者：
Li L;Yu X;Thompson A;Guo M;Yoshida S;Asami T;Chory J;Yin Y
植物激素生物学的一个悖论是一个小分子如何影响各种各样的生长和发育过程。例如，油菜素类固醇（BR）调节细胞伸长、维管分化、衰老和应激反应。BRs通过转录因子的BES 1/BZR 1（bri 1-EMS-抑制子1/阿喹唑耐药1）家族进行信号传导，该家族调节参与该途径的数百个靶基因;然而对该转录网络知之甚少。通过基因芯片和染色质免疫沉淀（ChIP）实验，我们鉴定了BES 1的一个直接靶基因AtMYB 30，它编码MYB家族转录因子。AtMYB 30无效突变体显示BR反应降低，并可增强BR受体突变体bri 1的弱等位基因的矮化表型。在AtMYB 30突变体中，许多BR调节基因的表达和/或凋亡诱导减少，表明AtMYB 30的功能是促进BR靶基因亚组的表达。AtMYB 30和BES 1分别与受BR和AtMYB 30调控的基因启动子中的保守MYB结合位点和E-box序列结合。AtMYB 30和BES 1在体内外都能相互作用。这些结果表明，BES 1和AtMYB 30协同作用，以促进BR靶基因的表达。因此，我们的研究结果建立了一种新的机制，通过这种机制，AtMYB 30，BES 1的直接靶点，通过帮助BES 1激活下游靶基因来放大BR信号。
A paradox of plant hormone biology is how a single small molecule can affect a diverse array of growth and developmental processes. For instance, brassinosteroids (BRs) regulate cell elongation, vascular differentiation, senescence and stress responses. BRs signal through the BES1/BZR1 (bri1-EMS-suppressor 1/Brassinazole-Resistant 1) family of transcription factors, which regulate hundreds of target genes involved in this pathway; yet little is known of this transcriptional network. By microarray and chromatin immunoprecipitation (ChIP) experiments, we identified a direct target gene of BES1, AtMYB30, which encodes a MYB family transcription factor. AtMYB30 null mutants display decreased BR responses and can enhance the dwarf phenotype of a weak allele of the BR receptor mutant bri1. Many BR-regulated genes have reduced expression and/or hormone-induction in AtMYB30 mutants, indicating that AtMYB30 functions to promote the expression of a subset of BR-target genes. AtMYB30 and BES1 bind to a conserved MYB-binding site and E-box sequences, respectively, in the promoters of genes that are regulated by both BRs and AtMYB30. Finally, AtMYB30 and BES1 interact with each other both in vitro and in vivo. These results demonstrated that BES1 and AtMYB30 function cooperatively to promote BR target gene expression. Our results therefore establish a new mechanism by which AtMYB30, a direct target of BES1, functions to amplify BR signaling by helping BES1 activate downstream target genes.