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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211319 | GEO | 2023/05/16

REPOSITORIES: GEO

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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [RNA-seq]

Project description:Erythroid genes having enhancers in a short distance appear to be transcriptionally activated by histone H3K27ac extension and intergenic transcription that are independent from TAL1.

2023-05-16 | GSE211316 | GEO

Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [ChIP-seq]

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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner

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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [RNA-seq]

Project description:Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [RNA-seq]

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Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [ChIP-seq]

Project description:Histone H3K27ac extension and intergenic transcription from enhancers activate close erythroid genes in a TAL1-independent manner [ChIP-seq]

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Genome-wide maps of GATA1, TAL1, and H3K27ac occupancy in erythroid precursors

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Histone H3K27ac separates active from poised enhancers and predicts developmental state.

Project description:Developmental programs are controlled by transcription factors and chromatin regulators, which maintain specific gene expression programs through epigenetic modification of the genome. These regulatory events at enhancers contribute to the specific gene expression programs that determine cell state and the potential for differentiation into new cell types. Although enhancer elements are known to be associated with certain histone modifications and transcription factors, the relationship of these modifications to gene expression and developmental state has not been clearly defined. Here we interrogate the epigenetic landscape of enhancer elements in embryonic stem cells and several adult tissues in the mouse. We find that histone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements containing H3K4me1 alone. This indicates that the amount of actively used enhancers is lower than previously anticipated. Furthermore, poised enhancer networks provide clues to unrealized developmental programs. Finally, we show that enhancers are reset during nuclear reprogramming.

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A dynamic H3K27ac signature identifies VEGFA-stimulated endothelial enhancers and requires EP300 activity.

Project description:Histone modifications are now well-established mediators of transcriptional programs that distinguish cell states. However, the kinetics of histone modification and their role in mediating rapid, signal-responsive gene expression changes has been little studied on a genome-wide scale. Vascular endothelial growth factor A (VEGFA), a major regulator of angiogenesis, triggers changes in transcriptional activity of human umbilical vein endothelial cells (HUVECs). Here, we used chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) to measure genome-wide changes in histone H3 acetylation at lysine 27 (H3K27ac), a marker of active enhancers, in unstimulated HUVECs and HUVECs stimulated with VEGFA for 1, 4, and 12 h. We show that sites with the greatest H3K27ac change upon stimulation were associated tightly with EP300, a histone acetyltransferase. Using the variation of H3K27ac as a novel epigenetic signature, we identified transcriptional regulatory elements that are functionally linked to angiogenesis, participate in rapid VEGFA-stimulated changes in chromatin conformation, and mediate VEGFA-induced transcriptional responses. Dynamic H3K27ac deposition and associated changes in chromatin conformation required EP300 activity instead of altered nucleosome occupancy or changes in DNase I hypersensitivity. EP300 activity was also required for a subset of dynamic H3K27ac sites to loop into proximity of promoters. Our study identified thousands of endothelial, VEGFA-responsive enhancers, demonstrating that an epigenetic signature based on the variation of a chromatin feature is a productive approach to define signal-responsive genomic elements. Further, our study implicates global epigenetic modifications in rapid, signal-responsive transcriptional regulation.

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Luminal lncRNAs Regulation by ER?-Controlled Enhancers in a Ligand-Independent Manner in Breast Cancer Cells.

Project description:Estrogen receptor-? (ER?) is a ligand-inducible protein which mediates estrogenic hormones signaling and defines the luminal BC phenotype. Recently, we demonstrated that even in absence of ligands ER? (apoER?) binds chromatin sites where it regulates transcription of several protein-coding and lncRNA genes. Noteworthy, apoER?-regulated lncRNAs marginally overlap estrogen-induced transcripts, thus representing a new signature of luminal BC genes. By the analysis of H3K27ac enrichment in hormone-deprived MCF-7 cells, we defined a set of Super Enhancers (SEs) occupied by apoER?, including one mapped in proximity of the DSCAM-AS1 lncRNA gene. This represents a paradigm of apoER? activity since its expression is largely unaffected by estrogenic treatment, despite the fact that E2 increases ER? binding on DSCAM-AS1 promoter. We validated the enrichment of apoER?, p300, GATA3, FoxM1 and CTCF at both DSCAM-AS1 TSS and at its associated SE by ChIP-qPCR. Furthermore, by analyzing MCF-7 ChIA-PET data and by 3C assays, we confirmed long range chromatin interaction between the SE and the DSCAM-AS1 TSS. Interestingly, CTCF and p300 binding showed an enrichment in hormone-depleted medium and in the presence of ER?, elucidating the dynamics of the estrogen-independent regulation of DSCAM-AS1 expression. The analysis of this lncRNA provides a paradigm of transcriptional regulation of a luminal specific apoER? regulated lncRNA.

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