• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >Multiple Roles for the MyoD Basic Region in Transmission of Transcriptional Activation Signals and Interaction with MEF2
【24h】

Multiple Roles for the MyoD Basic Region in Transmission of Transcriptional Activation Signals and Interaction with MEF2

机译：MyoD基本区域在转录激活信号的传递和与MEF2相互作用中的多重作用

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Establishment of skeletal muscle lineages is controlled by the MyoD family of basic helix-loop-helix (bHLH) transcription factors. The ability of these factors to initiate myogenesis is dependent on two conserved amino acid residues, alanine and threonine, in the basic domains of these factors. It has been postulated that these two residues may be responsible for the initiation of myogenesis via interaction with an essential myogenic cofactor. The myogenic bHLH proteins cooperatively activate transcription and myogenesis through protein-protein interactions with members of the myocyte enhancer factor 2 (MEF2) family of MADS domain transcription factors. MyoD-E12 heterodimers interact with MEF2 proteins to synergistically activate myogenesis, while homodimers of E12, which lack the conserved alanine and threonine residues in the basic domain, do not interact with MEF2. We have examined whether the myogenic alanine and threonine in the MyoD basic region are required for interaction with MEF2. Here, we show that substitution of the MyoD basic domain with that of E12 does not prevent interaction with MEF2. Instead, the inability of alanine-threonine mutants of MyoD to initiate myogenesis is due to a failure to transmit transcriptional activation signals provided either from the MyoD or the MEF2 activation domain. This defect in transcriptional transmission can be overcome by substitution of the MyoD or the MEF2 activation domain with the VP16 activation domain. These results demonstrate that myogenic bHLH-MEF2 interaction can be uncoupled from transcriptional activation and support the idea that the myogenic residues in myogenic bHLH proteins are essential for transmission of a transcriptional activation signal.
机译：骨骼肌谱系的建立由基本螺旋-环-螺旋（bHLH）转录因子的MyoD家族控制。这些因素引发肌发生的能力取决于这些因素的基本域中两个保守的氨基酸残基，丙氨酸和苏氨酸。据推测，这两个残基可能通过与必需的成肌辅因子相互作用而引发肌发生。成肌bHLH蛋白通过与MADS域转录因子的肌细胞增强因子2（MEF2）家族成员的蛋白相互作用，共同激活转录和肌发生。 MyoD-E12异二聚体与MEF2蛋白相互作用以协同激活肌发生，而E12的同二聚体在基本域中缺乏保守的丙氨酸和苏氨酸残基，而与MEF2不相互作用。我们已经检查了与MEF2相互作用是否需要MyoD基本区域中的肌源性丙氨酸和苏氨酸。在这里，我们表明，用E12取代MyoD基本域不会阻止与MEF2的交互。取而代之的是，MyoD的丙氨酸-苏氨酸突变体无法启动肌发生是由于无法传递从MyoD或MEF2激活域提供的转录激活信号。可以通过用VP16激活域取代MyoD或MEF2激活域来克服转录传递中的这一缺陷。这些结果表明，成肌bHLH-MEF2相互作用可以与转录激活脱钩，并支持成肌bHLH蛋白中的成肌残基对于转录激活信号的传递至关重要。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号