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本文引用的文献

1
The Isw2 chromatin-remodeling ATPase cooperates with the Fkh2 transcription factor to repress transcription of the B-type cyclin gene CLB2.Isw2染色质重塑ATP酶与Fkh2转录因子协同作用,以抑制B型细胞周期蛋白基因CLB2的转录。
Mol Cell Biol. 2007 Apr;27(8):2848-60. doi: 10.1128/MCB.01798-06. Epub 2007 Feb 5.
2
Polo kinase controls cell-cycle-dependent transcription by targeting a coactivator protein.Polo激酶通过靶向一种共激活蛋白来控制细胞周期依赖性转录。
Nature. 2006 Nov 23;444(7118):494-8. doi: 10.1038/nature05339.
3
A dual role for PP1 in shaping the Msn2-dependent transcriptional response to glucose starvation.PP1在塑造对葡萄糖饥饿的Msn2依赖性转录反应中具有双重作用。
EMBO J. 2005 Dec 7;24(23):4115-23. doi: 10.1038/sj.emboj.7600871. Epub 2005 Nov 10.
4
Sin3: a flexible regulator of global gene expression and genome stability.Sin3:全局基因表达和基因组稳定性的灵活调节因子。
Curr Genet. 2005 Jan;47(1):1-17. doi: 10.1007/s00294-004-0541-5. Epub 2004 Nov 23.
5
Regulation of cell cycle-specific gene expression through cyclin-dependent kinase-mediated phosphorylation of the forkhead transcription factor Fkh2p.通过细胞周期蛋白依赖性激酶介导的叉头转录因子Fkh2p磷酸化对细胞周期特异性基因表达的调控。
Mol Cell Biol. 2004 Nov;24(22):10036-46. doi: 10.1128/MCB.24.22.10036-10046.2004.
6
Dynactin is involved in a checkpoint to monitor cell wall synthesis in Saccharomyces cerevisiae.动力蛋白激活蛋白参与了酿酒酵母中监测细胞壁合成的一个检查点。
Nat Cell Biol. 2004 Sep;6(9):861-71. doi: 10.1038/ncb1162. Epub 2004 Aug 15.
7
Targeted proteomic study of the cyclin-Cdk module.细胞周期蛋白 - 细胞周期蛋白依赖性激酶模块的靶向蛋白质组学研究
Mol Cell. 2004 Jun 18;14(6):699-711. doi: 10.1016/j.molcel.2004.05.025.
8
Precocious G1/S transitions and genomic instability: the origin connection.早熟的G1/S期转换与基因组不稳定:起源的联系。
Mutat Res. 2003 Nov 27;532(1-2):5-19. doi: 10.1016/j.mrfmmm.2003.08.006.
9
Cell cycle-regulated transcription through the FHA domain of Fkh2p and the coactivator Ndd1p.通过Fkh2p的FHA结构域和共激活因子Ndd1p进行的细胞周期调控转录。
Curr Biol. 2003 Sep 30;13(19):1740-5. doi: 10.1016/j.cub.2003.08.053.
10
Recruitment of Thr 319-phosphorylated Ndd1p to the FHA domain of Fkh2p requires Clb kinase activity: a mechanism for CLB cluster gene activation.将苏氨酸319磷酸化的Ndd1p招募至Fkh2p的FHA结构域需要Clb激酶活性:一种CLB簇基因激活机制。
Genes Dev. 2003 Jul 15;17(14):1789-802. doi: 10.1101/gad.1074103.

G2/M期特异性基因CLB2的激活需要多个细胞周期信号。

Activation of the G2/M-specific gene CLB2 requires multiple cell cycle signals.

作者信息

Veis J, Klug H, Koranda M, Ammerer G

机构信息

Max F. Perutz Laboratories, University Departments at the Vienna Biocenter, Department of Biochemistry, University of Vienna, Dr. Bohrgasse 9, 1030 Vienna, Austria.

出版信息

Mol Cell Biol. 2007 Dec;27(23):8364-73. doi: 10.1128/MCB.01253-07. Epub 2007 Oct 1.

DOI:10.1128/MCB.01253-07
PMID:17908798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2169163/
Abstract

In budding yeast (Saccharomyces cerevisiae), the periodic expression of the G2/M-specific gene CLB2 depends on a DNA binding complex that mediates its repression during G1 and activation from the S phase to the exit of mitosis. The switch from low to high expression levels depends on the transcriptional activator Ndd1. We show that the inactivation of the Sin3 histone deacetylase complex bypasses the essential role of Ndd1 in cell cycle progression. Sin3 and its catalytic subunit Rpd3 associate with the CLB2 promoter during the G1 phase of the cell cycle. Both proteins dissociate from the promoter at the onset of the S phase and reassociate during G2 phase. Sin3 removal coincides with a transient increase in histone H4 acetylation followed by the expulsion of at least one nucleosome from the promoter region. Whereas the first step depends on Cdc28/Cln1 activity, Ndd1 function is required for the second step. Since the removal of Sin3 is independent of Ndd1 recruitment and Cdc28/Clb activity it represents a unique regulatory step which is distinct from transcriptional activation.

摘要

在出芽酵母(酿酒酵母)中,G2/M特异性基因CLB2的周期性表达依赖于一种DNA结合复合物,该复合物在G1期介导其抑制作用,并在从S期到有丝分裂退出期间介导其激活作用。从低表达水平到高表达水平的转变取决于转录激活因子Ndd1。我们发现,Sin3组蛋白去乙酰化酶复合物的失活绕过了Ndd1在细胞周期进程中的关键作用。Sin3及其催化亚基Rpd3在细胞周期的G1期与CLB2启动子结合。这两种蛋白质在S期开始时从启动子上解离,并在G2期重新结合。Sin3的去除与组蛋白H4乙酰化的短暂增加同时发生,随后至少一个核小体从启动子区域被驱逐。虽然第一步依赖于Cdc28/Cln1活性,但第二步需要Ndd1发挥作用。由于Sin3的去除独立于Ndd1的募集和Cdc28/Clb活性,它代表了一个独特的调控步骤,与转录激活不同。