...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Nucleus >L1 retrotransposition is activated by Ten-eleven-translocation protein 1 and repressed by methyl-CpG binding proteins
【24h】

L1 retrotransposition is activated by Ten-eleven-translocation protein 1 and repressed by methyl-CpG binding proteins

机译：L1逆转座子由十一个11易位蛋白1激活并被甲基CpG结合蛋白抑制

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

摘要

One of the major functions of DNA methylation is the repression of transposable elements, such as the long-interspersed nuclear element 1 (L1). The underlying mechanism(s), however, are unclear. Here, we addressed how retrotransposon activation and mobilization are regulated by methyl-cytosine modifying ten-eleven-translocation (Tet) proteins and how this is modulated by methyl-CpG binding domain (MBD) proteins. We show that Tet1 activates both, endogenous and engineered L1 retrotransposons. Furthermore, we found that Mecp2 and Mbd2 repress Tet1-mediated activation of L1 by preventing 5hmC formation at the L1 promoter. Finally, we demonstrate that the methyl-CpG binding domain, as well as the adjacent non-sequence specific DNA binding domain of Mecp2 are each sufficient to mediate repression of Tet1-induced L1 mobilization. Our study reveals a mechanism how L1 elements get activated in the absence of Mecp2 and suggests that Tet1 may contribute to Mecp2/Mbd2-deficiency phenotypes, such as the Rett syndrome. We propose that the balance between methylation “reader” and “eraser/writer” controls L1 retrotransposition.
机译：DNA甲基化的主要功能之一是抑制转座因子，例如长时间散布的核元素1（L1）。但是，底层机制还不清楚。在这里，我们讨论了如何通过甲基胞嘧啶修饰十一个十一易位（Tet）蛋白来调节反转录转座子的激活和动员，以及如何通过甲基CpG结合域（MBD）蛋白来调节逆转座子的激活和动员。我们显示，Tet1激活内源性和工程L1逆转座子。此外，我们发现Mecp2和Mbd2通过防止在L1启动子处形成5hmC来抑制Tet1介导的L1激活。最后，我们证明了Mecp2的甲基CpG结合域以及相邻的非序列特异性DNA结合域均足以介导Tet1诱导的L1动员的抑制。我们的研究揭示了在没有Mecp2的情况下L1元素如何被激活的机制，并暗示Tet1可能有助于Mecp2 / Mbd2缺乏型，例如Rett综合征。我们建议甲基化“读取器”和“擦除器/写入器”之间的平衡控制L1的逆转座。

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