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Genome-wide profiling of H3K27ac (ChIP-seq) in IMR90 cells

ABSTRACT: To determine the genome-wide pattern of H3K27ac in IMR90 (ATCC CCL-186) cells we performed ChIP-seq upon hormone treatment (1.5 h, 1 M dexamethasone).

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Homo sapiens

SUBMITTER: Robert Schpflin

PROVIDER: E-MTAB-5355 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genomic dissection of enhancers uncovers principles of combinatorial regulation and cell type-specific wiring of enhancer-promoter contacts.

Thormann Verena V Rothkegel Maika C MC Schöpflin Robert R Glaser Laura V LV Djuric Petar P Li Na N Chung Ho-Ryun HR Schwahn Kevin K Vingron Martin M Meijsing Sebastiaan H SH

Nucleic acids research 20180401 6

Genomic binding of transcription factors, like the glucocorticoid receptor (GR), is linked to the regulation of genes. However, as we show here, GR binding is a poor predictor of GR-dependent gene regulation even when taking the 3D organization of the genome into account. To connect GR binding sites to the regulation of genes in the endogenous genomic context, we turned to genome editing. By deleting GR binding sites, individually or in combination, we uncovered how cooperative interactions betw ...[more]

PMID: 29385519

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ChIP-sequencing analysis of Myc binding sites 4 hours after Myc activation in liver and heart tissue, from wild type and R26CAG-c-MycERT2 mice

Project description:Aim: To determine Myc binding sites in mouse heart and liver, 4 hours post MycER activation. c-Myc ChIP sequencing performed on chromatin isolated from hearts and livers harvested from wild-type (R26+/+) and R26CAG-c-MycERT2/+ mice 4 hours post administration of (Z)-4-hydroxytamoxifen.

2020-02-24 | E-MTAB-7592 | biostudies-arrayexpress

ChIP-sequencing analysis of RNA Pol II binding sites 4 hours after Myc activation in liver and heart tissue, from wild type and R26CAG-c-MycERT2 mice

Project description:Aim: To determine RNA Pol II binding sites in mouse heart and liver, 4 hours post MycER activation. Pol II ChIP sequencing performed on chromatin isolated from hearts and livers harvested from wild-type (R26+/+) and R26CAG-c-MycERT2/+ mice 4 hours post administration of (Z)-4-hydroxytamoxifen.

2020-03-06 | E-MTAB-7593 | biostudies-arrayexpress

Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [ChIP-seq_Input]

Project description:Polycomb group (PcG) proteins are required for normal differentiation and development, and their activity is found deregulated in cancer. PcG proteins are involved in gene silencing, however, whether they initiate or maintain transcriptional repression is a subject of debate. Here, we show that knockout of the Polycomb repressive complex 2 (PRC2) does not lead to significant gene expression changes in mouse embryonic stem cells (mESCs), and that it is dispensable for initiating silencing of target genes during differentiation. Transcriptional inhibition in mESCs is sufficient to induce genome-wide ectopic PRC2 recruitment to endogenous PcG target genes found in other tissues. PRC2 binding analysis shows that it is restricted to nucleosome-free CpG islands (CGIs) of un-transcribed genes. Our results show that it is the transcriptional state that governs PRC2 binding, and we propose that it binds by default to non-transcribed CGI genes to maintain their silenced state and to protect cell identity. Input from ChIP-seq experiment in Mus musculus wild-type E14 Embryonic Stem Cells.

2014-07-03 | E-GEOD-58022 | biostudies-arrayexpress

Histone deacetylase 3 in concert with MeCP2 and FoxO regulate autism-associated behaviors.

Project description:ChIP-Seq data of HDAC3 in mouse C57BL/6J hippocampus and RNA-Seq data of hippocampal CA1 in control and HDAC3c KO mice. NGS ChIP-Seq and RNA-Seq profiling of mouse hippocampus

2016-07-01 | E-GEOD-72196 | biostudies-arrayexpress

Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [ChIP-seq_drugs]

Project description:Polycomb group (PcG) proteins are required for normal differentiation and development, and their activity is found deregulated in cancer. PcG proteins are involved in gene silencing, however, whether they initiate or maintain transcriptional repression is a subject of debate. Here, we show that knockout of the Polycomb repressive complex 2 (PRC2) does not lead to significant gene expression changes in mouse embryonic stem cells (mESCs), and that it is dispensable for initiating silencing of target genes during differentiation. Transcriptional inhibition in mESCs is sufficient to induce genome-wide ectopic PRC2 recruitment to endogenous PcG target genes found in other tissues. PRC2 binding analysis shows that it is restricted to nucleosome-free CpG islands (CGIs) of un-transcribed genes. Our results show that it is the transcriptional state that governs PRC2 binding, and we propose that it binds by default to non-transcribed CGI genes to maintain their silenced state and to protect cell identity. Suz12, H3K27me3 and RNAPII ChIP-seq experiments before and after transcriptional inhibition with either DRB (0h, 6h and 12h) or Triptolide (0h, 3h and 9h) treatment of Mus musculus wild-type E14 Embryonic Stem Cells with up to two biological replicates per condition.

2014-07-03 | E-GEOD-58019 | biostudies-arrayexpress

Deletion of KDM2B DNA-binding domain affects RING1B and SUZ12 occupancy

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2014-05-27 | E-GEOD-52619 | biostudies-arrayexpress

Deletion of RING1A/B and loss of H2AK119ub1 affects PRC2 occupancy and H3K27me3 genome-wide

Project description:The chromatin modifying activities inherent to polycomb repressive complexes PRC1 and PRC2 play an essential role in gene regulation, cellular differentiation, and development. However, the mechanisms by which these complexes recognize their target sites and function together to form repressive chromatin domains remain poorly understood. Recruitment of PRC1 to target sites has been proposed to occur through a hierarchical process, dependent on the prior nucleation of PRC2 and placement of H3K27me3. Here, using a de novo targeting assay in mouse embryonic stem cells we unexpectedly discover that PRC1-dependent H2AK119ub1 leads to the recruitment of PRC2 and H3K27me3 to effectively initiate a polycomb domain. Genetic ablation of catalytic subunit of the PRC1 complex (RINGA/B) and ChIP-seq analysis of PRC1 and PRC2 components confirmed genome-wide decreases in PRC2 occupancy and H3K27me3 levels at PRC target sites. This activity is restricted to variant PRC1 complexes and genetic ablation experiments reveal that targeting of the variant PCGF1/PRC1 complex by KDM2B to CpG islands is required for polycomb domain formation and normal development. Together these observations provide a surprising new PRC1-dependent logic for PRC2 occupancy and polycomb domain formation. RING1A-/-;RING1Bfl/fl ES cells were treated with 800M-BM-5M tamoxifen for 48hours and compared to untreated control cells by ChIP-seq for RING1B, SUZ12, EZH2 and H3K27me3.

2014-05-27 | E-GEOD-55697 | biostudies-arrayexpress

Nanoscale Chromatin Profiling of Gastric Adenocarcinoma

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2014-07-30 | E-GEOD-51776 | biostudies-arrayexpress

Co-ordinate inhibition of autism candidate genes by topoisomerase inhibitors [Seq]

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2013-08-30 | E-GEOD-43526 | biostudies-arrayexpress

Impact of Tcf1 and Lef1 deficiency on histone marks and Tcf1 binding in CD8 T cells

Project description:Comparison of epigenome and Tcf1 occupancy between control and Tcf1/Lef1-deficient CD8 T cells Control mice or those are deficient for Tcf1 and Lef1 transcription factors (deleted by CD4-Cre) were used to isolate thymocytes. The thymocytes were surface-stained to identify TCRbeta high, CD69â, CD24â CD8+ subsets. These cells were sorted for ChIPseq analysis of various histone marks. Control mice or those are deficient for Tcf1 (deleted by CD4-Cre) were used to isolate thymocytes. The splenocytes were surface-stained to identify TCRbeta high, CD8+ subsets. These cells were sorted for ChIPseq analysis of Tcf1 binding locations.

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