• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >NF-E2 disrupts chromatin structure at human beta-globin locus control region hypersensitive site 2 in vitro.
【24h】

NF-E2 disrupts chromatin structure at human beta-globin locus control region hypersensitive site 2 in vitro.

机译：NF-E2在体外破坏人β-珠蛋白基因座控制区超敏位点2的染色质结构。

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

摘要

The human beta-globin locus control region (LCR) is responsible for forming an active chromatin structure extending over the 100-kb locus, allowing expression of the beta-globin gene family. The LCR consists of four erythroid-cell-specific DNase I hypersensitive sites (HS1 to -4). DNase I hypersensitive sites are thought to represent nucleosome-free regions of DNA which are bound by trans-acting factors. Of the four hypersensitive sites only HS2 acts as a transcriptional enhancer. In this study, we examine the binding of an erythroid protein to its site within HS2 in chromatin in vitro. NF-E2 is a transcriptional activator consisting of two subunits, the hematopoietic cell-specific p45 and the ubiquitous DNA-binding subunit, p18. NF-E2 binds two tandem AP1-like sites in HS2 which form the core of its enhancer activity. In this study, we show that when bound to in vitro-reconstituted chromatin, NF-E2 forms a DNase I hypersensitive site at HS2 similar to the site observed in vivo. Moreover, NF-E2 binding in vitro results in a disruption of nucleosome structure which can be detected 200 bp away. Although NF-E2 can disrupt nucleosomes when added to preformed chromatin, the disruption is more pronounced when NF-E2 is added to DNA prior to chromatin assembly. Interestingly, the hematopoietic cell-specific subunit, p45, is necessary for binding to chromatin but not to naked DNA. Interaction of NF-E2 with its site in chromatin-reconstituted HS2 allows a second erythroid factor, GATA-1, to bind its nearby sites. Lastly, nucleosome disruption by NF-E2 is an ATP-dependent process, suggesting the involvement of energy-dependent nucleosome remodeling factors.
机译：人β-珠蛋白基因座控制区（LCR）负责形成一个延伸超过100-kb基因座的活性染色质结构，从而表达β-珠蛋白基因家族。 LCR由四个类红细胞特异性DNase I超敏位点（HS1至-4）组成。 DNase I超敏位点被认为代表了由反式作用因子结合的DNA的无核小体区域。在四个超敏位点中，仅HS2充当转录增强子。在这项研究中，我们检查了类红细胞蛋白与其在染色质中HS2内的位点的结合。 NF-E2是一种转录激活因子，由两个亚基组成，即造血细胞特异性p45和普遍存在的DNA结合亚基p18。 NF-E2与HS2中的两个串联AP1样位点结合，形成其增强子活性的核心。在这项研究中，我们显示当与体外重组染色质结合时，NF-E2在HS2上会形成DNase I超敏位点，类似于体内观察到的位点。此外，NF-E2体外结合导致核小体结构的破坏，可以在200 bp处检测到。尽管将NF-E2添加到预先形成的染色质中时可以破坏核小体，但是当在染色质组装之前将NF-E2添加到DNA中时，这种破坏更为明显。有趣的是，造血细胞特异的亚基p45是结合染色质而不是裸DNA所必需的。 NF-E2与其在染色质重构的HS2中的位点相互作用，使第二类红细胞因子GATA-1与其附近位点结合。最后，NF-E2破坏核小体是一个ATP依赖的过程，这表明参与了能量依赖的核小体重塑因子。

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