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TEA转录因子Tec1通过依赖Ste12和不依赖Ste12的机制赋予启动子特异性基因调控。

The TEA transcription factor Tec1 confers promoter-specific gene regulation by Ste12-dependent and -independent mechanisms.

作者信息

Heise Barbara, van der Felden Julia, Kern Sandra, Malcher Mario, Brückner Stefan, Mösch Hans-Ulrich

机构信息

Philipps-Universität Marburg, Department of Genetics, Marburg, Germany.

出版信息

Eukaryot Cell. 2010 Apr;9(4):514-31. doi: 10.1128/EC.00251-09. Epub 2010 Jan 29.

Abstract

In Saccharomyces cerevisiae, the TEA transcription factor Tec1 is known to regulate target genes together with a second transcription factor, Ste12. Tec1-Ste12 complexes can activate transcription through Tec1 binding sites (TCSs), which can be further combined with Ste12 binding sites (PREs) for cooperative DNA binding. However, previous studies have hinted that Tec1 might regulate transcription also without Ste12. Here, we show that in vivo, physiological amounts of Tec1 are sufficient to stimulate TCS-mediated gene expression and transcription of the FLO11 gene in the absence of Ste12. In vitro, Tec1 is able to bind TCS elements with high affinity and specificity without Ste12. Furthermore, Tec1 contains a C-terminal transcriptional activation domain that confers Ste12-independent activation of TCS-regulated gene expression. On a genome-wide scale, we identified 302 Tec1 target genes that constitute two distinct classes. A first class of 254 genes is regulated by Tec1 in a Ste12-dependent manner and is enriched for genes that are bound by Tec1 and Ste12 in vivo. In contrast, a second class of 48 genes can be regulated by Tec1 independently of Ste12 and is enriched for genes that are bound by the stress transcription factors Yap6, Nrg1, Cin5, Skn7, Hsf1, and Msn4. Finally, we find that combinatorial control by Tec1-Ste12 complexes stabilizes Tec1 against degradation. Our study suggests that Tec1 is able to regulate TCS-mediated gene expression by Ste12-dependent and Ste12-independent mechanisms that enable promoter-specific transcriptional control.

摘要

在酿酒酵母中,已知TEA转录因子Tec1与另一个转录因子Ste12共同调节靶基因。Tec1-Ste12复合物可通过Tec1结合位点(TCS)激活转录,这些位点可进一步与Ste12结合位点(PRE)结合以实现协同DNA结合。然而,先前的研究暗示Tec1也可能在没有Ste12的情况下调节转录。在这里,我们表明在体内,生理量的Tec1足以在没有Ste12的情况下刺激TCS介导的基因表达和FLO11基因的转录。在体外,Tec1能够在没有Ste12的情况下以高亲和力和特异性结合TCS元件。此外,Tec1含有一个C末端转录激活结构域,可赋予TCS调节的基因表达以不依赖Ste12的激活。在全基因组范围内,我们鉴定出302个Tec1靶基因,它们构成两个不同的类别。第一类254个基因由Tec1以依赖Ste12的方式调节,并且在体内富含被Tec1和Ste12结合的基因。相比之下,第二类48个基因可由Tec1独立于Ste12进行调节,并且富含被应激转录因子Yap6、Nrg1、Cin5、Skn7、Hsf1和Msn4结合的基因。最后,我们发现Tec1-Ste12复合物的组合控制可稳定Tec1以防止其降解。我们的研究表明,Tec1能够通过依赖Ste12和不依赖Ste12的机制调节TCS介导的基因表达,从而实现启动子特异性转录控制。

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