Removal of histone tails from nucleosome dissects the physical mechanisms of salt-induced aggregation, linker histone H1-induced compaction, and 30-nm fiber formation of the nucleosome array
Removal of histone tails from nucleosome dissects the physical mechanisms of salt-induced aggregation, linker histone H1-induced compaction, and 30-nm fiber formation of the nucleosome array
复制标题
DOI：
10.1016/j.ultramic.2009.03.014
复制
发表时间：
2009-07-01
期刊：
影响因子：
2.2
通讯作者：
Takeyasu, Kunio
中科院分区：
文献类型：
--
作者：
Hizume, Kohji;Nakai, Tonau;Takeyasu, Kunio
为了揭示组蛋白尾部在形成高级染色质结构中的作用，我们采用原子力显微镜（AFM）和体外重建系统来研究由无尾组蛋白和长DNA（106-kb质粒）模板组成的重建染色质的性质。无尾核小体在高盐浓度下或与过量的核心组蛋白一起不聚集，与由含有正常N-末端尾的核小体组成的核小体阵列的行为相反。对我们的核小体分布的分析表明，无尾核小体之间的吸引相互作用减弱。在无尾核小体阵列中加入连接蛋白H1不能促进通常在正常核小体阵列中形成的30 nm染色质纤维的形成。这些结果表明，核小体之间通过组蛋白尾部的吸引相互作用在均匀的30 nm染色质纤维的形成中起着关键作用。(c)2009爱思唯尔有限公司版权所有。
In order to reveal the roles of histone tails in the formation of higher-order chromatin structures, we employed atomic force microscopy (AFM), and an in vitro reconstitution system to examine the properties of reconstituted chromatin composed of tail-less histones and a long DNA (106-kb plasmid) template. The tail-less nucleosomes did not aggregate at high salt concentrations or with an excess amount of core histones, in contrast with the behavior of nucleosomal arrays composed of nucleosomes containing normal, N-terminal tails. Analysis of our nucleosome distributions reveals that the attractive interaction between tail-less nucleosomes is weakened. Addition of linker histone H1 into the tail-less nucleosomal array failed to promote the formation of 30 nm chromatin fibers that are usually formed in the normal nucleosomal array. These results demonstrate that the attractive interaction between nucleosomes via histone tails plays a critical role in the formation of the uniform 30-nm chromatin fiber. (c) 2009 Elsevier B.V. All rights reserved.