Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA190041 | ENA |
REPOSITORIES: ENA
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Project description:TFIID and SAGA complexes play a critical role in RNA Polymerase II dependent activated transcription. Although the two regulatory complexes are recruited to promoters by activation domain-interactions, the contribution of the different subunits or the different domains of the individual subunits is not completely understood. Taf9 is a shared subunit in TFIID and SAGA and has an N-terminal H3-like histone fold domain and a highly conserved C-terminal domain, Taf9-CTD. In this study, we have uncovered an essential role for the Taf9-CTD in transcriptional activation. The Taf9-CTD was not essential for the histone-fold mediated interaction with Taf6, SAGA and TFIID integrity or Gcn4 interaction with SAGA. Transcriptome profiling performed under Gcn4 activating conditions showed that the Taf9-CTD is required for expression of ~17% of the yeast genome and provides a coactivator function to recruit TFIID and SAGA complexes to the promoters in vivo during transcriptional activation. Integrated genome-wide data analysis showed that the Taf9-CTD is required for activation of promoters bound by several transcription factors indicating a broad role for Taf9-CTD in promoter occupancy of TFIID or SAGA complexes. Interestingly, only a subset of the promoters seemed to be dependent on the Taf9-CTD for assembly of the pre-initiation complex indicating redundancy in activator targets to assemble PIC in vivo. Together these results indicate that evolutionarily conserved domains in shared subunits of TFIID and SAGA have a pervasive role in genome-wide transcription. This GEO series consists of 14 microarray hybridizations using the Agilent two-color experiment with the Agilent Custom Saccharomyces cerevisiae 8x15k gene expression array. Four biological replicates each for the wild-type (TAF9), the mutant taf9-tCRD2 strain treated or untreated with SM, and the wild-type (TAF9) versus mutant taf9-tCRD2 treated with SM hybridized as dye-swapped replicates. Two biological replicates for wild-type (SPT20) vs spt20D strains treated with SM, and hybridized as dye-swapped replicates to identify the fraction of SAGA dependent genes under amino-acid starvation conditions. The overall aim was to identify genes dependent on the conserved C-terminal region domain of TAF9 and determine their dependence on the SAGA subunit Spt20 for expression.
2014-02-21 | E-GEOD-44544 | biostudies-arrayexpress
Project description:TFIID and SAGA complexes play a critical role in RNA Polymerase II dependent activated transcription. Although the two regulatory complexes are recruited to promoters by activation domain-interactions, the contribution of the different subunits or the different domains of the individual subunits is not completely understood. Taf9 is a shared subunit in TFIID and SAGA and has an N-terminal H3-like histone fold domain and a highly conserved C-terminal domain, Taf9-CTD. In this study, we have uncovered an essential role for the Taf9-CTD in transcriptional activation. The Taf9-CTD was not essential for the histone-fold mediated interaction with Taf6, SAGA and TFIID integrity or Gcn4 interaction with SAGA. Transcriptome profiling performed under Gcn4 activating conditions showed that the Taf9-CTD is required for expression of ~17% of the yeast genome and provides a coactivator function to recruit TFIID and SAGA complexes to the promoters in vivo during transcriptional activation. Integrated genome-wide data analysis showed that the Taf9-CTD is required for activation of promoters bound by several transcription factors indicating a broad role for Taf9-CTD in promoter occupancy of TFIID or SAGA complexes. Interestingly, only a subset of the promoters seemed to be dependent on the Taf9-CTD for assembly of the pre-initiation complex indicating redundancy in activator targets to assemble PIC in vivo. Together these results indicate that evolutionarily conserved domains in shared subunits of TFIID and SAGA have a pervasive role in genome-wide transcription.
2014-02-21 | GSE44544 | 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:Organisms respond to heat stress by reprogramming gene expression. Here we show that genome-wide reprogramming involves enhanced assembly of the TFIID and SAGA regulatory pathways at heat induced genes, and disassembly of the TFIID pathway at heat-repressed genes. While TFIID and SAGA are recruited to heat-induced genes, only SAGA appears to be associated with achieving maximal induction. Mot1, an ATP-dependent inhibitor of the TATA binding protein TBP, assembles at heat-induced SAGA-regulated genes, but functions to attenuate rather than promote activation. Changes in promoter occupancy of bromodomain factor Bdf1 are tightly linked to changes in TFIID occupancy, which further supports the notion that the two work together. Bdf1 is inhibitory to a number of SAGA-regulated genes and dissociates when these genes are activated, suggesting that Bdf1 normally blocks transcription complex assembly at these genes. These linkages in reprogramming of factor occupancy at promoters provide direct evidence for two functionally distinct transcription assembly pathways, and reveal unexpected cross-talk between the pathways. Keywords = Chromatin Immunoprecipitation Keywords = Microarray Keywords = TBP
2010-06-05 | E-GEOD-1373 | 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
2004-02-26 | E-GEOD-885 | biostudies-arrayexpress
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:The conserved multi-subunit Ccr4-Not complex regulates gene expression in diverse ways. In this work, we characterize the suppression of temperature sensitivity associated with a mutation in the gene encoding the scaffold subunit of the Ccr4-Not complex, NOT1, by the deletion of SPT3. We determine that the deletion of SPT3, but not the deletion of genes encoding other subunits of the SAGA complex, globally suppresses transcriptional defects of not1-2. We find that transcriptional activation in not1-2 is associated with increased binding of TFIID and SAGA at promoters of upregulated genes, and this is suppressed by the deletion of SPT3. Interestingly, Spt3p-dependent activation of transcription occurs in not1-2 even if the SAGA complex is disrupted by the deletion of SPT7 that encodes a subunit of SAGA required for its integrity. Consistent with a SAGA-independent function of Spt3p, the deletion of SPT3 displays synthetic phenotypes when combined with a deletion of SPT7. Taken together, our results provide a new view of the Spt3 protein by identifying a SAGA-independent function of this protein that is functionally linked to the Ccr4-Not complex. Experiment Overall Design: 4 strains were analyzed: the wild type reference strain, two simple mutants (not1-2 and spt3) and one double mutant (not1-2 spt3). All strains were in duplicate.
2008-06-16 | E-GEOD-9432 | biostudies-arrayexpress
Project description:The SAGA co-activator complex contains distinct chromatin-modifying activities and is recruited by DNA-bound activators to regulate the expression of a subset of genes. Surprisingly, recent studies revealed little overlap between genome-wide SAGA-binding profiles and changes in gene expression upon depletion of subunits of the complex. As indicators of SAGA recruitment on chromatin, we monitored in yeast and human cells the genome-wide distribution of histone H3K9 acetylation and H2B ubiquitination, which are respectively deposited or removed by SAGA. Changes in these modifications after inactivation of the corresponding enzyme revealed that SAGA acetylates the promoters and deubiquitinates the transcribed region of all expressed genes. In agreement with this broad distribution, we show that SAGA plays a critical role for RNA polymerase II recruitment at all expressed genes. In addition, through quantification of newly synthesized RNA, we demonstrated that SAGA inactivation induced a strong decrease of mRNA synthesis at all tested genes. Analysis of the SAGA deubiquitination activity further revealed that SAGA acts on the whole transcribed genome in a very fast manner indicating a highly dynamic association of the complex with chromatin. Thus, our study uncovers a new function for SAGA as a bone fide co-factor for all RNA Polymerase II transcription. Comparison of H3K9ac, H2Bub and RNA Pol II distributions in WT yeast cells and upon the loss of SAGA activities.
2014-08-29 | E-GEOD-52997 | biostudies-arrayexpress
Project description:The SAGA co-activator complex contains distinct chromatin-modifying activities and is recruited by DNA-bound activators to regulate the expression of a subset of genes. Surprisingly, recent studies revealed little overlap between genome-wide SAGA-binding profiles and changes in gene expression upon depletion of subunits of the complex. As indicators of SAGA recruitment on chromatin, we monitored in yeast and human cells the genome-wide distribution of histone H3K9 acetylation and H2B ubiquitination, which are respectively deposited or removed by SAGA. Changes in these modifications after inactivation of the corresponding enzyme revealed that SAGA acetylates the promoters and deubiquitinates the transcribed region of all expressed genes. In agreement with this broad distribution, we show that SAGA plays a critical role for RNA polymerase II recruitment at all expressed genes. In addition, through quantification of newly synthesized RNA, we demonstrated that SAGA inactivation induced a strong decrease of mRNA synthesis at all tested genes. Analysis of the SAGA deubiquitination activity further revealed that SAGA acts on the whole transcribed genome in a very fast manner indicating a highly dynamic association of the complex with chromatin. Thus, our study uncovers a new function for SAGA as a bone fide co-factor for all RNA Polymerase II transcription. Comparison of H3K9ac and H2Bub distributions in control HeLa cells and upon the inactivation of SAGA enzymatic activities
2014-08-29 | E-GEOD-52860 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. The SAGA co-activator complex contains distinct chromatin-modifying activities and is recruited by DNA-bound activators to regulate the expression of a subset of genes. Surprisingly, recent studies revealed little overlap between genome-wide SAGA-binding profiles and changes in gene expression upon depletion of subunits of the complex. As indicators of SAGA recruitment on chromatin, we monitored in yeast and human cells the genome-wide distribution of histone H3K9 acetylation and H2B ubiquitination, which are respectively deposited or removed by SAGA. Changes in these modifications after inactivation of the corresponding enzyme revealed that SAGA acetylates the promoters and deubiquitinates the transcribed region of all expressed genes. In agreement with this broad distribution, we show that SAGA plays a critical role for RNA polymerase II recruitment at all expressed genes. In addition, through quantification of newly synthesized RNA, we demonstrated that SAGA inactivation induced a strong decrease of mRNA synthesis at all tested genes. Analysis of the SAGA deubiquitination activity further revealed that SAGA acts on the whole transcribed genome in a very fast manner indicating a highly dynamic association of the complex with chromatin. Thus, our study uncovers a new function for SAGA as a bone fide co-factor for all RNA Polymerase II transcription. Refer to individual Series
2014-08-29 | E-GEOD-59370 | biostudies-arrayexpress