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组蛋白伴侣Asf1提高了酵母PHO5和PHO8启动子处组蛋白移除的速率。

The histone chaperone Asf1 increases the rate of histone eviction at the yeast PHO5 and PHO8 promoters.

作者信息

Korber Philipp, Barbaric Slobodan, Luckenbach Tim, Schmid Andrea, Schermer Ulrike J, Blaschke Dorothea, Hörz Wolfram

机构信息

Adolf-Butenandt-Institut, Universität München, Schillerstrasse 44, 80336 Münich, Germany.

出版信息

J Biol Chem. 2006 Mar 3;281(9):5539-45. doi: 10.1074/jbc.M513340200. Epub 2006 Jan 4.

Abstract

Eukaryotic gene expression starts off from a largely obstructive chromatin substrate that has to be rendered accessible by regulated mechanisms of chromatin remodeling. The yeast PHO5 promoter is a well known example for the contribution of positioned nucleosomes to gene repression and for extensive chromatin remodeling in the course of gene induction. Recently, the mechanism of this remodeling process was shown to lead to the disassembly of promoter nucleosomes and the eviction of the constituent histones in trans. This finding called for a histone acceptor in trans and thus made histone chaperones likely to be involved in this process. In this study we have shown that the histone chaperone Asf1 increases the rate of histone eviction at the PHO5 promoter. In the absence of Asf1 histone eviction is delayed, but the final outcome of the chromatin transition is not affected. The same is true for the coregulated PHO8 promoter where induction also leads to histone eviction and where the rate of histone loss is reduced in asf1 strains as well, although less severely. Importantly, the final extent of chromatin remodeling is not affected. We have also presented evidence that Asf1 and the SWI/SNF chromatin remodeling complex work in distinct parallel but functionally overlapping pathways, i.e. they both contribute toward the same outcome without being mutually strictly dependent.

摘要

真核基因表达起始于一种高度致密的染色质底物,必须通过染色质重塑的调控机制使其变得可及。酵母PHO5启动子是一个著名的例子,它展示了定位核小体对基因抑制的作用以及基因诱导过程中广泛的染色质重塑。最近,这种重塑过程的机制被证明会导致启动子核小体的解体以及组成型组蛋白的反式驱逐。这一发现表明需要一个反式组蛋白受体,因此使得组蛋白伴侣蛋白可能参与这一过程。在本研究中,我们表明组蛋白伴侣蛋白Asf1提高了PHO5启动子处组蛋白驱逐的速率。在没有Asf1的情况下,组蛋白驱逐会延迟,但染色质转变的最终结果不受影响。对于共调控的PHO8启动子也是如此,其诱导也会导致组蛋白驱逐,并且在asf1菌株中组蛋白丢失的速率也会降低,尽管程度较轻。重要的是,染色质重塑的最终程度不受影响。我们还提供了证据表明Asf1和SWI/SNF染色质重塑复合体在不同但功能重叠的平行途径中起作用,即它们都朝着相同的结果做出贡献,而不是相互严格依赖。

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