...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >Position-dependent transcriptional regulation of the murine dihydrofolate reductase promoter by the E2F transactivation domain.
【24h】

Position-dependent transcriptional regulation of the murine dihydrofolate reductase promoter by the E2F transactivation domain.

机译：E2F反式激活域对鼠二氢叶酸还原酶启动子的位置依赖性转录调控。

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

摘要

Activity of the dihydrofolate reductase (dhfr) promoter increases at the G1-S-phase boundary of the cell cycle. Mutations that abolish protein binding to an E2F element in the dhfr promoter also abolish the G1-S-phase increase in dhfr transcription, indicating that transcriptional regulation is mediated by the E2F family of proteins. To investigate the mechanism by which E2F regulates dhfr transcription, we moved the E2F element upstream and downstream of its natural position in the promoter. We found that the E2F element confers growth regulation to the dhfr promoter only when it is proximal to the transcription start site. Using a heterologous E2F element, we showed that position-dependent regulation is a property that is promoter specific, not E2F element specific. We demonstrated that E2F-mediated growth regulation of dhfr transcription requires activation of the dhfr promoter in S phase and that the C-terminal activation domains of E2F1, E2F4, and E2F5, when fused to the Gal4 DNA binding domain, are sufficient to specify position-dependent activation. To further investigate the role of activation in dhfr regulation, we tested other transactivation domains for their ability to activate the dhfr promoter. We found that the N-terminal transactivation domain of VP16 cannot activate the dhfr promoter. We propose that, unlike other E2F-regulated promoters, robust transcription from the dhfr promoter requires an E2F transactivation domain close to the transcription start site.
机译：二氢叶酸还原酶（dhfr）启动子的活性在细胞周期的G1-S期边界增加。取消与dhfr启动子中E2F元素结合的蛋白质的突变也消除了dhfr转录的G1-S期增加，这表明转录调控是由E2F蛋白质家族介导的。为了研究E2F调节dhfr转录的机制，我们将E2F元件移动到其在启动子中自然位置的上游和下游。我们发现E2F元素仅在dhfr启动子接近转录起始位点时才赋予生长调节作用。使用异源E2F元素，我们证明了位置依赖性调控是启动子特异性而不是E2F元素特异性的特性。我们证明E2F介导的dhfr转录的生长调节需要在S期激活dhfr启动子，并且当与Gal4 DNA结合结构域融合时，E2F1，E2F4和E2F5的C端激活结构域足以确定位置依赖性激活。为了进一步研究激活在dhfr调控中的作用，我们测试了其他反式激活域激活dhfr启动子的能力。我们发现，VP16的N末端反式激活结构域不能激活dhfr启动子。我们建议，与其他E2F调控的启动子不同，从dhfr启动子进行的强健转录需要靠近转录起始位点的E2F反式激活域。

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