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Replicational dilution of H3K27me3 in mammalian cells and the role of poised promoters

ABSTRACT: Replicational dilution of H3K27me3 in mammalian cells and the role of poised promoters

PROVIDER: PRJNA528482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10546712_1.fastq.gz	Fastqsanger.gz
	SRR10546712_2.fastq.gz	Fastqsanger.gz
	SRR10546713_1.fastq.gz	Fastqsanger.gz
	SRR10546713_2.fastq.gz	Fastqsanger.gz
	SRR10546714_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Replicational Dilution of H3K27me3 in Mammalian Cells and the Role of Poised Promoters.

Project description:Polycomb repressive complex 2 (PRC2) places H3K27me3 at developmental genes and is causally implicated in keeping bivalent genes silent. It is unclear if that silence requires minimum H3K27me3 levels and how the mark transmits faithfully across mammalian somatic cell generations. Mouse intestinal cells lacking EZH2 methyltransferase reduce H3K27me3 proportionately at all PRC2 target sites, but ∼40% uniform residual levels keep target genes inactive. These genes, derepressed in PRC2-null villus cells, remain silent in intestinal stem cells (ISCs). Quantitative chromatin immunoprecipitation and computational modeling indicate that because unmodified histones dilute H3K27me3 by 50% each time DNA replicates, PRC2-deficient ISCs initially retain sufficient H3K27me3 to avoid gene derepression. EZH2 mutant human lymphoma cells also require multiple divisions before H3K27me3 dilution relieves gene silencing. In both cell types, promoters with high basal H3K4me2/3 activate in spite of some residual H3K27me3, compared to less-poised promoters. These findings have implications for PRC2 inhibition in cancer therapy.

| S-EPMC7376365 | biostudies-literature

Replicational dilution of H3K27me3 in mammalian cells and the role of poised promoters

Project description:Differential effect of PRC2 loss on gene repression in intestinal stem cells, transit amplifying cells, and differentiated villus cells in intestine is explained by disparity in the rate of cell division and resulting difference in H3K27me3 loss.

2020-01-17 | GSE128671 | GEO

H3K4me1 distribution at promoters predicts the poised epigenetic state

Project description:Post-translational modifications on histone tails are closely correlated to transcriptional states. One such modification is monomethylation on lysine 4 of histone 3(H3K4me1), a mark that has been linked to enhancers. Identifying regions enriched for H3K4me1 and depleted in H3K4me3, or regions enriched for both H3K4me1 and H3K27ac, has proven to be a feasible enhancer discovery method. At the same time, not all H3K4me1-enriched regions correspond to enhancers. H3K4me1 marks also exist at promoters, which implies that the H3K4me1 modification may have a context-dependent role in regulating transcription. We report distinct patterns of H3K4me1 that predict transcriptional regulatory states at promoters in germ cells and ESCs. We examined ChIP-seq data for H3K4me1, H3K4me3, H3K27me3, and H3K27ac in mouse and human male germ cells, and found that H3K4me1 peak density around the transcription start sites (TSS) exhibits either a broad bimodal profile or a narrower unimodal profile centered at the TSS. We then examined the position of the H3K4me1 marks relative to H3K4me3, and found that unimodal H3K4me1 directly at the TSS predicts a poised (H3K4me1/H3K27me3 bivalent) state of chromatin, while bimodal H3K4me1 flanking the TSS predicts an active state. We conclude that unimodal H3K4me1 centered on the TSS is a characteristic feature of the poised epigenetic state in ESCs and germ cells. Note: H3K4me1 and H3K27ac data are included in this GEO accession; H3K4me3 and H3K27me3 were released in GSE68507.

2020-04-05 | GSE145225 | GEO

Cross-species comparison of epigenetic poising in the mammalian germ line

Project description:In the mouse, germ cells and embryonic stem cells maintain an epigenetically poised (bivalent) state, defined by the simultaneous presence of the opposing histone modifications H3K4me3 and H3K27me3 and by transcriptional repression, at the promoters of many developmental regulatory genes. We compared genome-wide chromatin state in male germ cells of five mammalian and one avian species. We identified a set of 405 genes whose promoters retain poised chromatin in the mammalian germ line throughout mammalian evolution.

2016-05-07 | GSE68507 | GEO

H3K4me1 distribution at promoters predicts the poised epigenetic state

Project description:H3K4me1 distribution at promoters predicts the poised epigenetic state

| PRJNA606462 | ENA

Repurposing of promoters and enhancers during mammalian evolution

Project description:Repurposing of promoters and enhancers during mammalian evolution

| PRJNA470431 | ENA

An integrated SAGA and TFIID PIC assembly pathway selective for poised and induced promoters [ChIP-Exo]

Project description:Genome-wide, little is understood about how proteins organize at inducible promoters before and after in-duction, and to what extent inducible and constitutive architectures depend on cofactors. We report that se-quence-specific transcription factors and their tethered cofactors (e.g., SAGA, Mediator, TUP, NuA4, SWI/SNF, RPD3-L) are already bound to promoters prior to induction (“poised”), rather than recruited upon induction, whereas induction recruits the pre-initiation complex (PIC). Through depletion and/or deletion ex-periments we show that SAGA does not function at constitutive promoters, although a SAGA-independent Gcn5 does acetylate +1 nucleosomes there. At poised promoters, SAGA catalyzes +1 nucleosome acetylation but not PIC assembly. At induced promoters, SAGA catalyzes acetylation, deubiquitylation, and PIC assembly. Surprisingly, SAGA mediates induction by creating a PIC that allows TFIID to stably associate, rather than creating a TFIID-independent PIC, as is generally thought. These findings suggest that inducible systems, where present, evolved on top of constitutive systems.

2022-10-27 | GSE212654 | GEO

An integrated SAGA and TFIID PIC assembly pathway selective for poised and induced promoters [RNA-Seq]

2022-10-27 | GSE212653 | GEO

H3.3K27M mutant proteins reprogram epigenome by sequestering the PRC2 complex to poised enhancers

Project description:Expression of histone H3.3K27M mutant proteins in diffuse intrinsic pontine glioma (DIPG) results in a global reduction of tri-methylation of H3K27 (H3K27me3), and paradoxically, H3K27me3 peaks remain at hundreds of genomic loci, a dichotomous change that lacks mechanistic insights. Here we show that the PRC2 complex is sequestered at poised enhancers, but not at active promoters with high levels of H3.3K27M proteins, thereby contributing to the global reduction of H3K27me3. Moreover, the levels of H3.3K27M proteins are low at the retained H3K27me3 peaks and consequently having minimal effects on the PRC2 activity at these loci. H3K27me3-mediated silencing at specific tumor suppressor genes, including Wilms Tumor 1, promotes proliferation of DIPG cells. These results support a model in which the PRC2 complex is redistributed to poised enhancers in H3.3K27M mutant cells and supports the proliferation of DIPG cells in part through silencing of tumor suppressor gene WT1.

2018-07-02 | GSE94834 | GEO

Genome dilution by cell growth drives starvation-like proteome remodeling in mammalian and yeast cells

Project description:Cell size is tightly controlled in healthy tissues and single-celled organisms, but it remains unclear how cell size influences physiology. Increasing cell size was recently shown to remodel the proteomes of cultured human cells, demonstrating that large and small cells of the same type can be compositionally different. Here, we utilize the natural heterogeneity of hepatocyte ploidy and yeast genetics to establish that ploidy-to-cell size ratio is a highly conserved determinant of proteome composition. In both mammalian and yeast cells, genome dilution by cell growth elicits a starvation-like phenotype, suggesting that growth in large cells is restricted by genome concentration in manner that mimics a limiting nutrient. Moreover, genome dilution explains some proteomic changes ascribed to yeast aging. Overall, our data indicate that genome concentration drives changes in cell composition independently of external environmental cues.

2024-06-05 | GSE269091 | GEO

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