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本文引用的文献

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Chromatin topology is coupled to Polycomb group protein subnuclear organization.染色质拓扑结构与多梳蛋白亚核组织相关联。
Nat Commun. 2016 Jan 13;7:10291. doi: 10.1038/ncomms10291.
2
The E3 ubiquitin ligase activity of RING1B is not essential for early mouse development.RING1B的E3泛素连接酶活性对于小鼠早期发育并非必不可少。
Genes Dev. 2015 Sep 15;29(18):1897-902. doi: 10.1101/gad.268151.115.
3
Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation.在缺乏H2A单泛素化的情况下,PRC1介导的转录抑制作用
Genes Dev. 2015 Jul 15;29(14):1487-92. doi: 10.1101/gad.265439.115.
4
An ultra-low-input native ChIP-seq protocol for genome-wide profiling of rare cell populations.一种超低输入本底的免疫共沉淀测序(ChIP-seq)技术,用于对稀有细胞群体进行全基因组分析。
Nat Commun. 2015 Jan 21;6:6033. doi: 10.1038/ncomms7033.
5
HTSeq--a Python framework to work with high-throughput sequencing data.HTSeq——一个用于处理高通量测序数据的Python框架。
Bioinformatics. 2015 Jan 15;31(2):166-9. doi: 10.1093/bioinformatics/btu638. Epub 2014 Sep 25.
6
PRC1 complex diversity: where is it taking us?PRC1 复合物多样性:它将把我们带向何方?
Trends Cell Biol. 2014 Nov;24(11):632-41. doi: 10.1016/j.tcb.2014.06.005. Epub 2014 Jul 22.
7
Transcriptional regulation by Polycomb group proteins.多梳蛋白家族通过转录进行调控。
Nat Struct Mol Biol. 2013 Oct;20(10):1147-55. doi: 10.1038/nsmb.2669.
8
SAM domain polymerization links subnuclear clustering of PRC1 to gene silencing.SAM 结构域聚合将 PRC1 的亚核聚类与基因沉默联系起来。
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9
A histone mutant reproduces the phenotype caused by loss of histone-modifying factor Polycomb.一个组蛋白突变体能再现由组蛋白修饰因子 Polycomb 缺失引起的表型。
Science. 2013 Feb 8;339(6120):698-9. doi: 10.1126/science.1231382.
10
Compaction of chromatin by diverse Polycomb group proteins requires localized regions of high charge.各种 Polycomb 组蛋白通过压缩染色质需要局部高电荷区域。
Genes Dev. 2011 Oct 15;25(20):2210-21. doi: 10.1101/gad.17288211.

核小体压缩区域的突变会破坏多梳蛋白介导的轴向模式形成。

Mutation of a nucleosome compaction region disrupts Polycomb-mediated axial patterning.

作者信息

Lau Mei Sheng, Schwartz Matthew G, Kundu Sharmistha, Savol Andrej J, Wang Peggy I, Marr Sharon K, Grau Daniel J, Schorderet Patrick, Sadreyev Ruslan I, Tabin Clifford J, Kingston Robert E

机构信息

Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.

Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Science. 2017 Mar 10;355(6329):1081-1084. doi: 10.1126/science.aah5403. Epub 2017 Mar 9.

DOI:10.1126/science.aah5403
PMID:28280206
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5503153/
Abstract

Nucleosomes play important structural and regulatory roles by tightly wrapping the DNA that constitutes the metazoan genome. The Polycomb group (PcG) proteins modulate nucleosomes to maintain repression of key developmental genes, including genes whose temporal and spatial expression is tightly regulated to guide patterning of the anterior-posterior body axis. CBX2, a component of the mammalian Polycomb repressive complex 1 (PRC1), contains a compaction region that has the biochemically defined activity of bridging adjacent nucleosomes. Here, we demonstrate that a functional compaction region is necessary for proper body patterning, because mutating this region leads to homeotic transformations similar to those observed with PcG loss-of-function mutations. We propose that CBX2-driven nucleosome compaction is a key mechanism by which PcG proteins maintain gene silencing during mouse development.

摘要

核小体通过紧密包裹构成后生动物基因组的DNA发挥重要的结构和调节作用。多梳蛋白家族(PcG)蛋白调节核小体以维持关键发育基因的抑制状态,这些基因包括其时空表达受到严格调控以指导前后身体轴模式形成的基因。CBX2是哺乳动物多梳抑制复合物1(PRC1)的一个组成部分,包含一个压缩区域,该区域具有在生化上确定的桥接相邻核小体的活性。在这里,我们证明功能性压缩区域对于正确的身体模式形成是必需的,因为该区域的突变会导致同源异型转化,类似于PcG功能丧失突变所观察到的情况。我们提出,CBX2驱动的核小体压缩是PcG蛋白在小鼠发育过程中维持基因沉默的关键机制。