Histone chaperone Chz1 facilitates the disfavouring property of Spt16 to H2A.Z-containing genes in Saccharomyces cerevisiae
Histone chaperone Chz1 facilitates the disfavouring property of Spt16 to H2A.Z-containing genes in Saccharomyces cerevisiae
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组蛋白伴侣 Chz1 促进 Spt16 对酿酒酵母中含有 H2A.Z 的基因的不利特性
DOI：
10.1042/bj20140186
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发表时间：
2014
影响因子：
4.1
通讯作者：
Wan Yakun
中科院分区：
文献类型：
--
作者：
Liu Hongde;Luo Kun;Zhou Zikai;Mu Yawen;Wan Yakun
启动子处的Htz 1（组蛋白2A Z1）沉积参与静止基因的转录激活。Chz 1 [chaperone for Htz 1（or H2 A）-H2 B dimer]是一种Htz 1-H2 B特异性分子伴侣，可递送取代H2 A的组蛋白H2A.Z。Spt 16（Ty的抑制子）在转录延伸中起作用，并且还具有组蛋白伴侣活性。然而，Chz 1、Htz 1和Spt 16之间的联系仍然未知。在本研究中，我们确定的基因组结合分析的Htz 1，Pol II（RNA聚合酶II）和Spt 16使用ChIP微阵列实验和测序核小体DNA使用下一代测序技术在野生型和chz 1缺失菌株的酿酒酵母。本研究的结果表明，Spt 16和Pol II是相关的，结合在核小体耗尽区域，并与转录速率呈正相关。重要的是，Spt 16不赞成的Htz 1结合的基因，这种歧视是受损后删除的chz 1。Spt 16和Htz 1在启动子处的结合谱之间的负相关性不是内在排斥，而是可能由于转录起始的需要。我们发现chz 1缺失降低了启动子和端粒上的Htz 1结合。此外，在thechz 1缺失突变体，Spt 16结合在核糖体基因丢失。本研究的结果表明，Spt 16到Htz 1结合基因的歧视是由于Chz 1在Spt 16结合Htz 1结合基因组区域的优先权。因此，Chz 1护送的Htz 1损害了Spt 16在染色质上的结合。
Htz1 (histone 2A Z1) deposition at promoters is involved in the transcriptional activation of quiescent genes. Chz1 [chaperone for Htz1 (or H2A)–H2B dimer] is an Htz1–H2B-specific chaperone that delivers histone H2A.Z that substitutes for H2A. Spt16 (suppressor of Ty) functions in transcription elongation and also possesses a histone chaperone activity. However, the links among Chz1, Htz1 and Spt16 remain unknown. In the present study, we determined the genomic binding profiling of Htz1, Pol II (RNA polymerase II) and Spt16 using ChIP microarray experiments and sequenced nucleosomal DNA using a next-generation sequencing technique in wild-type andchz1-deletion strains ofSaccharomyces cerevisiae. The results of the present study revealed that Spt16 and Pol II are associated, bind at nucleosome-depleted regions, and are positively correlated with the transcription rate. Importantly, Spt16 disfavours the Htz1-bound genes, and this discrimination is impaired upon the deletion ofchz1. The negative correlation between the binding profiles of Spt16 and Htz1 at promoters is not an intrinsic repulsion, but is probably due to a requirement for transcription initiation. We showed thatchz1deletion decreases Htz1 binding at promoters and telomeres. Also, in thechz1-deletion mutant, Spt16 binding at ribosomal genes was lost. The results of the present study suggest that the discrimination of Spt16 to Htz1-bound genes is due to the priority of Chz1 over Spt16 in binding to the Htz1-bound genomic regions. Chz1-escorted Htz1 therefore impairs Spt16 binding at chromatin.