Genetic analysis argues for a coactivator function for the Saccharomyces cerevisiae Tup1 corepressor [ChIP-Seq]
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PROVIDER: PRJNA726878 | ENA |
REPOSITORIES: ENA
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Project description:The Tup1-Cyc8 corepressor complex of Saccharomyces cerevisiae is recruited to promoters by DNA-binding proteins to repress transcription of genes, including the a-specific mating type genes. We report here a tup1(S649F) mutant that displays mating irregularities similar to a tup1 null and an a-predominant growth defect. RNA-Seq and ChIP-Seq were used to analyze gene expression and Tup1 binding changes in mutant vs. wild-type in both a and a cells. Increased Tup1(S649F) binding tended to occur upstream of upregulated genes, whereas locations with decreased binding usually did not show changes in gene expression, suggesting this mutant not only loses corepressor function but also behaves as a coactivator. Based upon studies demonstrating a dual role of Tup1 in both repression and activation, we postulate that the coactivator function of Tup1(S649F) results from diminished interaction with repressor proteins, including a2. We also found that large changes in mating type-specific gene expression between a and a or between mutant and wild-type were not easily explained by the range of Tup1 binding levels within their promoters, as predicted by the classic model of a-specific gene repression by Tup1. Most surprisingly, we observed Tup1 binding upstream of the a-specific gene MFA2 and the a-specific gene MF(ALPHA)1 in cells in which each gene was expressed rather than repressed. These results, combined with identification of additional mating related genes upregulated in the tup1(S649F) a strain, illustrate that the role of Tup1 in distinguishing mating types in yeast appears to be both more comprehensive and more nuanced than previously appreciated.
2021-09-01 | GSE173721 | GEO
Project description:The Tup1-Cyc8 corepressor complex of Saccharomyces cerevisiae is recruited to promoters by DNA-binding proteins to repress transcription of genes, including the a-specific mating type genes. We report here a tup1(S649F) mutant that displays mating irregularities similar to a tup1 null and an a-predominant growth defect. RNA-Seq and ChIP-Seq were used to analyze gene expression and Tup1 binding changes in mutant vs. wild-type in both a and a cells. Increased Tup1(S649F) binding tended to occur upstream of upregulated genes, whereas locations with decreased binding usually did not show changes in gene expression, suggesting this mutant not only loses corepressor function but also behaves as a coactivator. Based upon studies demonstrating a dual role of Tup1 in both repression and activation, we postulate that the coactivator function of Tup1(S649F) results from diminished interaction with repressor proteins, including a2. We also found that large changes in mating type-specific gene expression between a and a or between mutant and wild-type were not easily explained by the range of Tup1 binding levels within their promoters, as predicted by the classic model of a-specific gene repression by Tup1. Most surprisingly, we observed Tup1 binding upstream of the a-specific gene MFA2 and the a-specific gene MF(ALPHA)1 in cells in which each gene was expressed rather than repressed. These results, combined with identification of additional mating related genes upregulated in the tup1(S649F) a strain, illustrate that the role of Tup1 in distinguishing mating types in yeast appears to be both more comprehensive and more nuanced than previously appreciated.
2021-09-01 | GSE173720 | GEO
Project description:Genetic analysis argues for a coactivator function for the Saccharomyces cerevisiae Tup1 corepressor
| PRJNA726875 | ENA
Project description:Genetic analysis argues for a coactivator function for the Saccharomyces cerevisiae Tup1 corepressor [RNA-Seq]
| PRJNA726877 | ENA
Project description:Saccharomyces cerevisiae normally cannot assimilate mannitol, a promising brown macroalgal carbon source for bioethanol production. To date, the molecular mechanisms underlying this inability remain unknown. Here, we found that cells acquiring mannitol-assimilating ability appeared from wild-type S. cerevisiae strain during prolonged culture in mannitol medium. Our microarray analysis revealed that genes for putative mannitol dehydrogenase and hexose transporters were up-regulated in cells acquiring mannitol-assimilating ability. Take account of our other results including complementation analysis and cell growth data, we demonstrated that this acquisition of mannitol-assimilating ability was due to the spontaneous mutation in the gene encoding Tup1 or Cyc8. Tup1-Cyc8 is the general corepressor complex involved in the repression of many kinds of genes. Thus, it is suggested that the inability of wild-type S. cerevisiae to assimilate mannitol can be attributed to the transcriptional repression of a set of genes involved in mannitol utilization by Tup1-Cyc8 corepressor. In other words, Tup1-Cyc8 is a key regulator of mannitol metabolism in S. cerevisiae. We also showed that S. cerevisiae strain which carries mutant allele of TUP1 or CYC8 produced ethanol from mannitol efficiently. Especially, strain carrying mutant allele of CYC8 showed high tolerance to salt, which is superior to other ethanologenic microorganisms. This characteristic is highly beneficial to produce bioethanol from marine biomass. Taken together, Tup1-Cyc8 can be an ideal target to develop a yeast-algal bioethanol production system. To figure out how Mtl+ strains (cells acquiring ability to grow in mannitol medium) had acquired the ability to assimilate mannitol, we performed genome-wide analysis by using Nimblegen microarrays. Yeast Saccharomyces cerevisiae cells (wild-type BY4742 strain and two Mtl+ strains, MK3619 and MK3683) were grown at 30°C to the logarithmic phase in SC or SM media. Total RNA was purified and the 4 RNA samples (BY4742 cells in SC as control, MK3619 cells in SM, MK3683 cells in both SC and SM) were analyzed with Nimblegen microarrays.
2014-12-04 | E-GEOD-55755 | biostudies-arrayexpress
Project description:Saccharomyces cerevisiae normally cannot assimilate mannitol, a promising brown macroalgal carbon source for bioethanol production. To date, the molecular mechanisms underlying this inability remain unknown. Here, we found that cells acquiring mannitol-assimilating ability appeared from wild-type S. cerevisiae strain during prolonged culture in mannitol medium. Our microarray analysis revealed that genes for putative mannitol dehydrogenase and hexose transporters were up-regulated in cells acquiring mannitol-assimilating ability. Take account of our other results including complementation analysis and cell growth data, we demonstrated that this acquisition of mannitol-assimilating ability was due to the spontaneous mutation in the gene encoding Tup1 or Cyc8. Tup1-Cyc8 is the general corepressor complex involved in the repression of many kinds of genes. Thus, it is suggested that the inability of wild-type S. cerevisiae to assimilate mannitol can be attributed to the transcriptional repression of a set of genes involved in mannitol utilization by Tup1-Cyc8 corepressor. In other words, Tup1-Cyc8 is a key regulator of mannitol metabolism in S. cerevisiae. We also showed that S. cerevisiae strain which carries mutant allele of TUP1 or CYC8 produced ethanol from mannitol efficiently. Especially, strain carrying mutant allele of CYC8 showed high tolerance to salt, which is superior to other ethanologenic microorganisms. This characteristic is highly beneficial to produce bioethanol from marine biomass. Taken together, Tup1-Cyc8 can be an ideal target to develop a yeast-algal bioethanol production system. To figure out how Mtl+ strains (cells acquiring ability to grow in mannitol medium) had acquired the ability to assimilate mannitol, we performed genome-wide analysis by using Nimblegen microarrays.
2014-12-04 | GSE55755 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE37465: Global Regulation of Nucleosome Organization And Transcription By The Yeast Ssn6-Tup1 Corepressor (MNase-Seq) GSE37466: Global Regulation of Nucleosome Organization And Transcription By The Yeast Ssn6-Tup1 Corepressor (expression) Refer to individual Series
2012-10-10 | E-GEOD-37467 | biostudies-arrayexpress
Project description:The yeast Ssn6-Tup1 complex regulates gene expression through a variety of mechanisms, including positioning of nucleosomes over promoters of some target genes to limit accessibility to the transcription machinery. To further define the functions of Ssn6-Tup1 in gene regulation and chromatin remodeling, we performed genome-wide profiling of changes in nucleosome organization and gene expression that occur upon loss of SSN6 or TUP1, and observed extensive nucleosome alterations in both promoters and gene bodies of derepressed genes. Our improved nucleosome profiling and analysis approaches revealed low-occupancy promoter nucleosomes (P nucleosomes) at locations previously defined as nucleosome-free regions. In the absence of SSN6 or TUP1, this P nucleosome is frequently lost, whereas nucleosomes are gained at -1 and +1 positions, accompanying up-regulation of downstream genes. Our analysis of public ChIP-seq data revealed that Ssn6 and Tup1 preferentially bind TATA-containing promoters, which are also enriched in genes derepressed upon loss of SSN6 or TUP1. These results suggest that stabilization of the P nucleosome on TATA-containing promoters may be a central feature of the repressive chromatin architecture created by the Ssn6-Tup1 corepressor, and that releasing the P nucleosome contributes to gene activation. Genome-wide expression profiling Yeast gene expression in three cell type, Each cell type is tested in duplicate.
2012-10-10 | E-GEOD-37466 | biostudies-arrayexpress
Project description:The yeast Ssn6-Tup1 complex regulates gene expression through a variety of mechanisms, including positioning of nucleosomes over promoters of some target genes to limit accessibility to the transcription machinery. To further define the functions of Ssn6-Tup1 in gene regulation and chromatin remodeling, we performed genome-wide profiling of changes in nucleosome organization and gene expression that occur upon loss of SSN6 or TUP1, and observed extensive nucleosome alterations in both promoters and gene bodies of derepressed genes. Our improved nucleosome profiling and analysis approaches revealed low-occupancy promoter nucleosomes (P nucleosomes) at locations previously defined as nucleosome-free regions. In the absence of SSN6 or TUP1, this P nucleosome is frequently lost, whereas nucleosomes are gained at -1 and +1 positions, accompanying up-regulation of downstream genes. Our analysis of public ChIP-seq data revealed that Ssn6 and Tup1 preferentially bind TATA-containing promoters, which are also enriched in genes derepressed upon loss of SSN6 or TUP1. These results suggest that stabilization of the P nucleosome on TATA-containing promoters may be a central feature of the repressive chromatin architecture created by the Ssn6-Tup1 corepressor, and that releasing the P nucleosome contributes to gene activation. nucleosomes were prepared from isogenic wild type (BY4742), ssn6 KO and tup1 KO cells after varying degrees of micrococcal nuclease (MNase) digestion, followed by isolation of mononucleosomal DNA and sequencing. Three replicates of each strain (9 samples) were subjected to Illumina sequencing.
2012-10-10 | E-GEOD-37465 | biostudies-arrayexpress
Project description:The yeast Ssn6-Tup1 complex regulates gene expression through a variety of mechanisms, including positioning of nucleosomes over promoters of some target genes to limit accessibility to the transcription machinery. To further define the functions of Ssn6-Tup1 in gene regulation and chromatin remodeling, we performed genome-wide profiling of changes in nucleosome organization and gene expression that occur upon loss of SSN6 or TUP1, and observed extensive nucleosome alterations in both promoters and gene bodies of derepressed genes. Our improved nucleosome profiling and analysis approaches revealed low-occupancy promoter nucleosomes (P nucleosomes) at locations previously defined as nucleosome-free regions. In the absence of SSN6 or TUP1, this P nucleosome is frequently lost, whereas nucleosomes are gained at -1 and +1 positions, accompanying up-regulation of downstream genes. Our analysis of public ChIP-seq data revealed that Ssn6 and Tup1 preferentially bind TATA-containing promoters, which are also enriched in genes derepressed upon loss of SSN6 or TUP1. These results suggest that stabilization of the P nucleosome on TATA-containing promoters may be a central feature of the repressive chromatin architecture created by the Ssn6-Tup1 corepressor, and that releasing the P nucleosome contributes to gene activation.
2012-10-10 | GSE37466 | GEO