Widespread binding of TFIID and SAGA to yeast promoters mapped by an improved ChEC-seq method
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PROVIDER: PRJNA549959 | ENA |
REPOSITORIES: ENA
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Project description:Deletions within genes coding for subunits of the transcription coactivator SAGA caused strong genome-wide defects in transcription and SAGA-mediated chromatin modifications. In contrast, rapid SAGA depletion produced only modest transcription defects at 13% of protein-coding genes – genes that are generally more sensitive to rapid TFIID depletion. However, transcription of these “coactivator-redundant” genes is strongly affected by rapid depletion of both factors, showing the overlapping functions of TFIID and SAGA at this gene set. We suggest that this overlapping function is linked to TBP-DNA recruitment. The remaining 87% of expressed genes that we term “TFIID-dependent” are highly sensitive to rapid TFIID depletion and insensitive to rapid SAGA depletion. Genome-wide mapping of SAGA and TFIID found binding of both factors at many genes independent of gene class. DNA analysis suggests that the distinction between the gene classes is due to multiple components rather than any single regulatory factor or promoter sequence motif.
2020-01-09 | GSE142120 | GEO
Project description:TFIID and SAGA share a common set of TAFs, regulate chromatin, and deliver TBP to promoters. Here we examine their relationship within the context of the Saccharomyces cerevisiae genome-wide regulatory network. We find that while TFIID and SAGA make overlapping contributions to the expression of all genes, TFIID function predominates at ~90% and SAGA at ~10% of the measurable genome. Strikingly, SAGA-dominated genes are largely stress-induced and TAF-independent, and are down-regulated by the coordinate action of a variety of chromatin, TBP, and RNA polymerase II regulators. In contrast, the TFIID-dominated class is less regulated, but is highly dependent upon TAFs including those shared between TFIID and SAGA. These two distinct modes of transcription regulation might reflect the need to balance inducible stress responses with the steady output of housekeeping genes. Keywords = Taf1 Keywords = Spt3 Keywords = Gcn5
2004-02-26 | E-GEOD-885 | biostudies-arrayexpress
Project description:TFIID and SAGA share a common set of TAFs, regulate chromatin, and deliver TBP to promoters. Here we examine their relationship within the context of the Saccharomyces cerevisiae genome-wide regulatory network. We find that while TFIID and SAGA make overlapping contributions to the expression of all genes, TFIID function predominates at ~90% and SAGA at ~10% of the measurable genome. Strikingly, SAGA-dominated genes are largely stress-induced and TAF-independent, and are down-regulated by the coordinate action of a variety of chromatin, TBP, and RNA polymerase II regulators. In contrast, the TFIID-dominated class is less regulated, but is highly dependent upon TAFs including those shared between TFIID and SAGA. These two distinct modes of transcription regulation might reflect the need to balance inducible stress responses with the steady output of housekeeping genes. Keywords = Taf1 Keywords = Spt3 Keywords = Gcn5 Keywords: other
2004-02-27 | GSE885 | GEO
Project description:Regulation of RNA polymerase II (RNAPII) transcription requires the concerted efforts of several multisubunit coactivator complexes, which interact with the RNAPII preinitiation complex (PIC) to stimulate transcription. We previously showed that separation of the Mediator core (cMed) from Mediator’s tail module results in modest overactivation of genes annotated as highly dependent on TFIID for expression. However, it is unclear if other coactivators are involved in this phenomenon. Here, we show that the overactivation of certain genes by cMed/tail separation is blunted by disruption of the SAGA complex through removal of its structural Spt20 subunit, though this downregulation does not appear to depend on reduced SAGA association with the genome. Consistent with the enrichment of TFIID-dependent genes among genes overactivated by cMed/tail separation, depletion of the essential TFIID subunit Taf13 suppressed overactivation of these genes when Med16 was simultaneously removed. As with SAGA, this effect did not appear to be dependent on reduced genomic association of TFIID. Given that the observed changes in gene expression could not be clearly linked to alterations in SAGA or TFIID occupancy, our data may suggest that the cMed/tail connection is important for modulation of SAGA and/or TFIID conformation and/or function at target genes.
2022-10-03 | GSE207369 | GEO
Project description:TFIID and SAGA are the only two known yeast complexes that modify chromatin and deliver TBP to promoters. Previous genome wide expression studies indicated that TFIID and SAGA positively regulate most but not all yeast genes. Using a relatively low noise microarray approach, we have re-examined the genome-wide dependence on TFIID and SAGA. We find that TFIID and SAGA contribute to the expression of virtually the entire genome, with TFIID being preferred at ~90% of the genes, and SAGA being preferred at ~10%. SAGA-dominated genes were found to overlap substantially with a previously described set of highly active genes that are attenuated in part by the TBP regulator NC2, and an auto-inhibitory function of TFIID. These SAGA-dominated genes also encompass most of the previously reported âTAF-independentâ genes. These results build upon and refine the generally held view that activators recruit either TFIID or SAGA to promoters which then bind and acetylate nucleosomes locally, thereby enhancing TBP delivery to the TATA box. Promoter-specific differences in the ability to alleviate auto-inhibitory activities associated with TFIID and SAGA might contribute to the preferential use one complex versus the other. Keywords = Chromatin Immunoprecipitation Keywords = genome-wide binding
2010-06-09 | E-GEOD-1061 | biostudies-arrayexpress
Project description:Deletions within genes coding for subunits of the transcription coactivator SAGA caused strong genome-wide defects in transcription and SAGA-mediated chromatin modifications. In contrast, rapid SAGA depletion produced only modest transcription defects at 13% of protein-coding genes – genes that are generally more sensitive to rapid TFIID depletion. However, transcription of these “coactivator-redundant” genes is strongly affected by rapid depletion of both factors, showing the overlapping functions of TFIID and SAGA at this gene set. We suggest that this overlapping function is linked to TBP-DNA recruitment. The remaining 87% of expressed genes that we term “TFIID-dependent” are highly sensitive to rapid TFIID depletion and insensitive to rapid SAGA depletion. Genome-wide mapping of SAGA and TFIID found binding of both factors at many genes independent of gene class. DNA analysis suggests that the distinction between the gene classes is due to multiple components rather than any single regulatory factor or promoter sequence motif.
2020-01-09 | GSE133004 | GEO
Project description:Deletions within genes coding for subunits of the transcription coactivator SAGA caused strong genome-wide defects in transcription and SAGA-mediated chromatin modifications. In contrast, rapid SAGA depletion produced only modest transcription defects at 13% of protein-coding genes – genes that are generally more sensitive to rapid TFIID depletion. However, transcription of these “coactivator-redundant” genes is strongly affected by rapid depletion of both factors, showing the overlapping functions of TFIID and SAGA at this gene set. We suggest that this overlapping function is linked to TBP-DNA recruitment. The remaining 87% of expressed genes that we term “TFIID-dependent” are highly sensitive to rapid TFIID depletion and insensitive to rapid SAGA depletion. Genome-wide mapping of SAGA and TFIID found binding of both factors at many genes independent of gene class. DNA analysis suggests that the distinction between the gene classes is due to multiple components rather than any single regulatory factor or promoter sequence motif.
2020-01-09 | GSE142183 | GEO
Project description:Deletions within genes coding for subunits of the transcription coactivator SAGA caused strong genome-wide defects in transcription and SAGA-mediated chromatin modifications. In contrast, rapid SAGA depletion produced only modest transcription defects at 13% of protein-coding genes – genes that are generally more sensitive to rapid TFIID depletion. However, transcription of these “coactivator-redundant” genes is strongly affected by rapid depletion of both factors, showing the overlapping functions of TFIID and SAGA at this gene set. We suggest that this overlapping function is linked to TBP-DNA recruitment. The remaining 87% of expressed genes that we term “TFIID-dependent” are highly sensitive to rapid TFIID depletion and insensitive to rapid SAGA depletion. Genome-wide mapping of SAGA and TFIID found binding of both factors at many genes independent of gene class. DNA analysis suggests that the distinction between the gene classes is due to multiple components rather than any single regulatory factor or promoter sequence motif.
2020-01-09 | GSE142182 | GEO
Project description:TFIID and SAGA are the only two known yeast complexes that modify chromatin and deliver TBP to promoters. Previous genome wide expression studies indicated that TFIID and SAGA positively regulate most but not all yeast genes. Using a relatively low noise microarray approach, we have re-examined the genome-wide dependence on TFIID and SAGA. We find that TFIID and SAGA contribute to the expression of virtually the entire genome, with TFIID being preferred at ~90% of the genes, and SAGA being preferred at ~10%. SAGA-dominated genes were found to overlap substantially with a previously described set of highly active genes that are attenuated in part by the TBP regulator NC2, and an auto-inhibitory function of TFIID. These SAGA-dominated genes also encompass most of the previously reported “TAF-independent” genes. These results build upon and refine the generally held view that activators recruit either TFIID or SAGA to promoters which then bind and acetylate nucleosomes locally, thereby enhancing TBP delivery to the TATA box. Promoter-specific differences in the ability to alleviate auto-inhibitory activities associated with TFIID and SAGA might contribute to the preferential use one complex versus the other. Keywords = Chromatin Immunoprecipitation Keywords = genome-wide binding Keywords: other
2004-03-01 | GSE1061 | GEO
Project description:Two separate roles for the transcription coactivator SAGA and a set of genes redundantly regulated by TFIID and SAGA [ChEC-Seq]
| PRJNA595939 | ENA