H3K9ac ChIP-seq in WT, SAGA and ATAC mutant mouse embryonic stem cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE175903 | GEO | 2021/08/03
REPOSITORIES: GEO
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Project description:Assess chromatin accessibility in WT and mutant ES E14 strains using ATAC-seq. Mutant strains are depleted for subunits of the coactivator complexes SAGA (Supt7l KO) or ATAC (Yeats2, Zzz3) using constitutive knock-out (KO) or the auxin-inducible degron (AID) system.
2021-08-03 | GSE175902 | GEO
Project description:To analyse the genome-wide impact of inactivation of the ATAC or SAGA coactivator complexes on RNA polymerase II (Pol II) transcription, we purified newly synthesized RNA from mutant mouse embryonic stem (ES) cell lines in which subunits of ATAC (Yeats2, Zzz3) or SAGA (Supt7l) are inactivated or depleted. We also performed this analysis in mutant cell lines in which a subunit (Tada3) of the shared histone acetyltransferase activity of these two complexes is depleted. Newly synthesized RNA was purified following the 4sU labelling method (more details in extract protocol). For two wildtype samples, the total RNA input was also analysed.
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Project description:The biological mechanisms that sustain the vast blood production required for healthy life remain incompletely understood. To search for novel regulators of hematopoiesis, we performed a genome-wide in vivo hematopoietic stem and progenitor cell (HSPC)-based CRISPR knockout screen for regulators of hematopoiesis. We discovered SAGA complex members, including Tada2b and Taf5l, as key regulators of hematopoiesis. Loss of Tada2b or Taf5l strongly inhibited hematopoiesis in vivo, causing a buildup of immature hematopoietic cells in the bone marrow. The SAGA complex deposits histone H3 lysine 9 acetylation (H3K9ac) and removes histone H2B ubiquitination (H2Bub). Loss of Tada2b led to reductions in H3K9ac levels and altered H2Bub enrichment in HSPCs, implicating disruption of SAGA complex activity. This was associated with upregulation of interferon pathway genes, reduced mitochondrial activity, and increased megakaryocyte progenitor cell commitment. Loss of these factors also enhanced the cell outgrowth and the interferon pathway in an in vivo human myelodysplastic syndrome cell line model. In summary, this study has identified the SAGA complex as an important regulator of hematopoiesis.
2025-12-08 | GSE312126 | GEO
Project description:The biological mechanisms that sustain the vast blood production required for healthy life remain incompletely understood. To search for novel regulators of hematopoiesis, we performed a genome-wide in vivo hematopoietic stem and progenitor cell (HSPC)-based CRISPR knockout screen for regulators of hematopoiesis. We discovered SAGA complex members, including Tada2b and Taf5l, as key regulators of hematopoiesis. Loss of Tada2b or Taf5l strongly inhibited hematopoiesis in vivo, causing a buildup of immature hematopoietic cells in the bone marrow. The SAGA complex deposits histone H3 lysine 9 acetylation (H3K9ac) and removes histone H2B ubiquitination (H2Bub). Loss of Tada2b led to reductions in H3K9ac levels and altered H2Bub enrichment in HSPCs, implicating disruption of SAGA complex activity. This was associated with upregulation of interferon pathway genes, reduced mitochondrial activity, and increased megakaryocyte progenitor cell commitment. Loss of these factors also enhanced the cell outgrowth and the interferon pathway in an in vivo human myelodysplastic syndrome cell line model. In summary, this study has identified the SAGA complex as an important regulator of hematopoiesis.
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Project description:The biological mechanisms that sustain the vast blood production required for healthy life remain incompletely understood. To search for novel regulators of hematopoiesis, we performed a genome-wide in vivo hematopoietic stem and progenitor cell (HSPC)-based CRISPR knockout screen for regulators of hematopoiesis. We discovered SAGA complex members, including Tada2b and Taf5l, as key regulators of hematopoiesis. Loss of Tada2b or Taf5l strongly inhibited hematopoiesis in vivo, causing a buildup of immature hematopoietic cells in the bone marrow. The SAGA complex deposits histone H3 lysine 9 acetylation (H3K9ac) and removes histone H2B ubiquitination (H2Bub). Loss of Tada2b led to reductions in H3K9ac levels and altered H2Bub enrichment in HSPCs, implicating disruption of SAGA complex activity. This was associated with upregulation of interferon pathway genes, reduced mitochondrial activity, and increased megakaryocyte progenitor cell commitment. Loss of these factors also enhanced the cell outgrowth and the interferon pathway in an in vivo human myelodysplastic syndrome cell line model. In summary, this study has identified the SAGA complex as an important regulator of hematopoiesis.
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Project description:The SAGA (Spt-Ada-Gcn5 acetyltransferase) complex is an evolutionarily conserved, multifunctional co-activator complex, which has a critical role in histone acetylation, gene expression, and various developmental processes in eukaryotes. However, little is known about the composition and function of the SAGA complex in plants. Here, we found that the SAGA complex in Arabidopsis thaliana contains not only conserved subunits and but also four plant-specific subunits, including three homologous subunits, SCS1, SCS2A, and SCS2B (SCS1/2A/2B), and a TAF-like subunit, TAFL. We also found that a series of SAGA subunits are shared in yeast and/or metazoans but are absent in Arabidopsis. Mutations in the unique SAGA subunits SCS1/2A/2B lead to defective phenotypes similar to those caused by mutations in the conserved SAGA subunits HAG1 and ADA2B; these defective phenotypes include delayed juvenile-to-adult phase transition, late flowering, and increased trichome density. SCS1/2A/2B function in the SAGA complex to promote the transcription of development-related genes by facilitating histone H3 acetylation. The results suggest that, compared to SAGA complexes in other eukaryotes, the SAGA complex in plants has evolved unique features that are necessary for normal growth and development.
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Project description:ChIP-nexus performed in Kc167 cells for subunits of the SAGA coactivator complex;ChIP performed in ovary homogenate for subunits of the SAGA coactivator complex
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Project description:The Spt-Ada-Gcn5-acetyltransferase (SAGA) chromatin-modifying complex is a transcriptional coactivator that contains four different modules of subunits. The intact SAGA complex has been well characterized for its function in transcription regulation and development. However, little is known about the roles of individual modules within SAGA and if they have any SAGA independent functions. Here we demonstrate that the two enzymatic modules of Drosophila SAGA are differently required in oogenesis. Loss of the HAT activity blocks oogenesis, while loss of the DUB activity does not. However, the DUB module regulates a subset of genes in early embryogenesis and loss of the DUB subunits causes defects in embryogenesis. ChIP-seq analysis of ada2b, spt3, nonstop, and sgf11revealed that both the DUB and HAT modules bind most SAGA target genes even though many of these targets do not require the DUB module for expression. Furthermore, we found that the DUB module can bind to chromatin and regulate transcription independently of the rest of SAGA. Our results suggest that the DUB module has functions within SAGA as well as independent functions.
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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