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Defining genome architecture at base-pair resolution

机译：在基对分辨率下定义基因组架构

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摘要

In higher eukaryotes, many genes are regulated by enhancers that are 10(4)-10(6) base pairs (bp) away from the promoter. Enhancers contain transcription-factor-binding sites (which are typically around 7-22 bp), and physical contact between the promoters and enhancers is thought to be required to modulate gene expression. Although chromatin architecture has been mapped extensively at resolutions of 1 kilobase and above; it has not been possible to define physical contacts at the scale of the proteins that determine gene expression. Here we define these interactions in detail using a chromosome conformation capture method (Micro-Capture-C) that enables the physical contacts between different classes of regulatory elements to be determined at base-pair resolution. We find that highly punctate contacts occur between enhancers, promoters and CCCTC-binding factor (CTCF) sites and we show that transcription factors have an important role in the maintenance of the contacts between enhancers and promoters. Our data show that interactions between CTCF sites are increased when active promoters and enhancers are located within the intervening chromatin. This supports a model in which chromatin loop extrusion(1) is dependent on cohesin loading at active promoters and enhancers, which explains the formation of tissue-specific chromatin domains without changes in CTCF binding.
机译：在较高的真核时，许多基因由来自启动子的10（4）-10（6）碱基对（BP）的增强子调节。增强剂含有转录因子结合位点（通常为7-22bp左右），并且被认为是调节基因表达所需的启动子和增强剂之间的物理接触。虽然染色质架构在1千碱基和以上的分辨率下广泛映射;尚未在确定基因表达的蛋白质的刻度下定义物理触点。在这里，我们使用染色体构象捕获方法（微捕获-c）详细定义这些交互，其使得在基对分辨率下确定不同类别的调节元件之间的物理触点。我们发现增强剂，启动子和CCCTC结合因子（CTCF）位点之间发生高度点状接触，并且我们表明转录因子在维持增强剂和启动子之间的接触方面具有重要作用。我们的数据显示，当活性启动子和增强剂位于介入染色质中时，CTCF位点之间的相互作用增加。这支持一种模型，其中染色质环挤出（1）取决于活性启动子和增强剂的幼耳加载，这解释了组织特异性染色质域的形成而不改变CTCF结合。

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  • 来源
    《Nature》 |2021年第7865期|125-129|共5页
  • 作者

    Hua Peng; Badat Mohsin; Hanssen Lars L. P.; Hentges Lance D.; Crump Nicholas; Downes Damien J.; Jeziorska Danuta M.; Oudelaar A. Marieke; Schwessinger Ron; Taylor Stephen; Milne Thomas A.; Hughes Jim R.; Higgs Doug R.; Davies James O. J.;

  • 作者单位

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England|Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC WIMM Ctr Computat Biol Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Max Planck Inst Biophys Chem Gottingen Germany;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC WIMM Ctr Computat Biol Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England|Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC WIMM Ctr Computat Biol Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med Lab Gene Regulat Oxford England;

    Univ Oxford MRC Weatherall Inst Mol Med Radcliffe Dept Med MRC Mol Haematol Unit Oxford England;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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