30 nm chromatin fibre decompaction requires both H4-K16 acetylation and linker histone eviction

30 nm chromatin fibre decompaction requires both H4-K16 acetylation and linker histone eviction
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DOI:
10.1016/j.jmb.2008.04.050
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发表时间:
2008-09-12
影响因子:
5.6
通讯作者:
Rhodes, Daniela
Rhodes, Daniela
中科院分区:
生物学2区
文献类型:
--
作者:
Robinson, Philip J. J.;An, Woojin;Rhodes, Daniela

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染色质去致密化以允许接近DNA的机制在很大程度上是未知的。在这里,使用模型核小体阵列重组组蛋白八聚体,我们已经定义。单个组蛋白八聚体N-末端尾的相对贡献以及靶向组蛋白尾乙酰化对30 nm染色质纤维的压实状态的影响。这项研究超越了以前的研究,因为它是基于一个核小体阵列,这是非常长的(61个核小体),并含有化学计量浓度的结合接头组蛋白,这是必不可少的30 nm染色质纤维的形成。我们发现,压缩调节在两个步骤:引入H4乙酰化到30%,在K16抑制压缩到更大的程度比删除的H4 N-末端尾巴。通过去除连接体组蛋白实现进一步的解压缩。(C)2008爱思唯尔有限公司保留所有权利。
The mechanism by which chromatin is decondensed to permit access to DNA is largely unknown. Here, using a model nucleosome array reconstituted from recombinant histone octamers, we have defined. the relative contribution of the individual histone octamer N-terminal tails as well as the effect of a targeted histone tail acetylation on the compaction state of the 30 nm chromatin fiber. This study goes beyond previous studies as it is based on a nucleosome array that is very long (61 nucleosomes) and contains a stoichiometric concentration of bound linker histone, which is essential for the formation of the 30 nm chromatin fiber. We find that compaction is regulated in two steps: Introduction of H4 acetylated to 30%, on K16 inhibits compaction to a greater degree than deletion of the H4 N-terminal tail. Further decompaction is achieved by removal of the linker histone. (C) 2008 Elsevier Ltd. All rights reserved.