The TEA Transcription Factor Tec1 Confers Promoter-Specific Gene Regulation by Ste12-Dependent and -Independent Mechanisms

被引:23
作者
Heise, Barbara [1 ]
van der Felden, Julia [1 ]
Kern, Sandra [1 ]
Malcher, Mario [1 ]
Brueckner, Stefan [1 ]
Moesch, Hans-Ulrich [1 ]
机构
[1] Univ Marburg, Dept Genet, D-35043 Marburg, Germany
关键词
ACTIVATED PROTEIN-KINASE; YEAST STE12 PROTEIN; SACCHAROMYCES-CEREVISIAE; INVASIVE GROWTH; CELL-TYPE; SIGNALING SPECIFICITY; FILAMENTOUS-GROWTH; PSEUDOHYPHAL DIFFERENTIATION; DNA-BINDING; PHEROMONE;
D O I
10.1128/EC.00251-09
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:514 / 531
页数:18
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