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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >MYBL2 is a substrate of GSK3-like kinase BIN2 and acts as a corepressor of BES1 in brassinosteroid signaling pathway in Arabidopsis
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MYBL2 is a substrate of GSK3-like kinase BIN2 and acts as a corepressor of BES1 in brassinosteroid signaling pathway in Arabidopsis

机译：MYBL2是类GSK3激酶BIN2的底物，并在拟南芥中油菜素类固醇信号传导途径中作为BES1的核心抑制剂。

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摘要

Plant steroid hormones, brassinosteroids (BRs), play important roles in plants. BRs regulate the expression of several thousand genes, half of which are induced and the other half repressed by the hormone. BRs signal through plasma membrane-localized receptor kinase brassinosteroid-insensitive 1 (BRI1), BRI1-associated receptor kinase (BAK1), and several intermediates to regulate the protein levels, cellular localizations, and/or DNA binding of BRI1-EMS suppressor 1 (BES1)/brassinazole-resistant 1 (BZR1) family transcription factors. Although BES1 is known to interact with other transcription factors, histone-modifying enzymes, and transcription elongation factors to activate BR-induced genes, how BES1 mediates the BR-re-pressed gene expression is not known. Here, we show that BES1 interacts with myeloblastosis family transcription factor-like 2 (MYBL2), a transcription repressor, to down-regulate BR-repressed gene expression. The loss-of-function mybl2 mutant enhances the phenotype of a weak allele of bri1 and suppresses the constitutive BR-response phenotype of bes1-D. The results suggest that suppression of BR-repressed gene expression is required for optimal BR response. Moreover, MYBL2 is a substrate of glycogen synthase kinase 3 (GSK3)-like kinase brassinosteroid-insensitive 2 (BIN2), which has been well established as a negative regulator in the BR pathway by phosphorylating and inhibiting the functions of BES1/BZR1. Unlike BIN2 phosphorylation of BES1/BZR1 leading to protein degradation, BIN2 phosphorylation stabilizes MYBL2. Such dual role of phosphorylation has also been reported in WNT signaling pathway in which GSK3 phosphorylation destabilizes p-catenin and stabilizes Axin, a scaffolding protein facilitating the phosphorylation of p-catenin by GSK3. Our results thus establish the mechanisms for BR-repressed gene expression and the integration of BR signaling and BR transcriptional network.
机译：植物类固醇激素，油菜素类固醇（BRs）在植物中起重要作用。 BRs调节数千个基因的表达，其中一半被诱导，另一半被激素抑制。 BR通过质膜定位受体激酶油菜素类固醇不敏感1（BRI1），BRI1相关受体激酶（BAK1）以及几种中间体调节BRI1-EMS抑制剂1的蛋白水平，细胞定位和/或DNA结合，从而发出信号（ BES1）/耐菜青素1（BZR1）家族转录因子。尽管已知BES1与其他转录因子，组蛋白修饰酶和转录延伸因子相互作用以激活BR诱导的基因，但BES1如何介导BR抑制的基因表达尚不清楚。在这里，我们显示BES1与成纤维细胞增生病家族转录因子样2（MYBL2），转录抑制因子相互作用，以下调BR抑制的基因表达。功能丧失的mybl2突变体增强了bri1弱等位基因的表型，并抑制了bes1-D的本构性BR反应表型。结果表明，抑制BR阻抑的基因表达是最佳BR反应所必需的。此外，MYBL2是糖原合酶激酶3（GSK3）样激酶油菜素甾体不敏感2（BIN2）的底物，通过磷酸化和抑制BES1 / BZR1的功能，它已在BR途径中确立为负调节剂。与BES1 / BZR1的BIN2磷酸化导致蛋白质降解不同，BIN2的磷酸化可稳定MYBL2。这种磷酸化的双重作用也已在WNT信号传导途径中报道，其中GSK3磷酸化使p-catenin不稳定并稳定Axin（一种促进GSK3对p-catenin磷酸化的支架蛋白）。因此，我们的结果建立了BR抑制基因表达的机制以及BR信号传导和BR转录网络的整合。

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  • 来源
  • 作者

    Huaxun Ye; Lei Li; Hongqing Guo; Yanhai Yin;

  • 作者单位

    Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, IA 50011;

    Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, IA 50011 Department of Molecular Biology and Center for Computational and Integrative Biology, Massachusetts General Hospital Department of Genetics, Har- vard Medical School, Boston, MA 02114;

    Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, IA 50011;

    Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, IA 50011;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    transcription repression; protein stability; plant growth hormone signaling;

    机译：转录抑制蛋白质稳定性;植物生长激素信号;

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