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Genome-wide maps of EED and H3K27me3 binding genes in WT and HBL1 KO human induced pluripotent stem cells (hiPSCs).

ABSTRACT: Genome-wide maps of EED and H3K27me3 binding genes in WT and HBL1 KO human induced pluripotent stem cells (hiPSCs).

PROVIDER: PRJNA627955 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11607109_1.fastq.gz	Fastqsanger.gz
	SRR11607109_2.fastq.gz	Fastqsanger.gz
	SRR11607110_1.fastq.gz	Fastqsanger.gz
	SRR11607110_2.fastq.gz	Fastqsanger.gz
	SRR11607111_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Genome-wide maps of EED and H3K27me3 binding genes in WT and HBL1 KO human induced pluripotent stem cells (hiPSCs).

Project description:We reported loss of HBL1 lnRNA promoted cardiogenesis and the interaction of HBL1-EED in hiPSCs. Here we used specific EED and H3K27me3 antibodies to pull down their binding genomic DNAs in hiPSCs, respectively, which let us know the potential genes regulated by HBL1-EED-H3K27me3 during cardiogenesis. 1% Input samples were collected from the same samples after chromatin shearing.

2021-06-10 | GSE149323 | GEO

EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent

Project description:In proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PCR2 writing of H3K27me3 is mechanistically required for gene silencing. Here we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (Embryonic Ectoderm Development) inactivation in the postnatal heart (Eed CKO ) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in Eed CKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized Eed CKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.

2017-04-14 | GSE73771 | GEO

Transcriptional repression by non-canonical EED stimulation of histone deacetylase activity is required for heart maturation independently of H3K27me3 [RNA-seq for EED and HDAC rescue]

Project description:Through H3K27me3 and H3K27ac ChIP-seq and RNA-seq data in wile-tpye (WT) and EED-knockout (CKO) mouse cardiomyocytes, we unexpectedly uncovered a novel mechanism of PRC2-mediated gene repression. EED inactivation in the postnatal heart (EEDCKO) caused progressive, lethal dilated cardiomyopathy, with upregulation of components of the slow-twitch muscle gene program. Surprisingly, upregulation of these genes was not associated with their loss of H3K27me3, but rather with their gain of H3K27 acetylation (H3K27ac), an activating histone mark. Moreover, re-expression of EED in juvenile hearts rescued heart function and normalized H3K27ac, but not H3K27me3.

2017-04-14 | GSE89585 | GEO

Maternal Eed knockout causes loss of H3K27me3 imprinting and random X-inactivation in the extra-embryonic cells

Project description:Genomic imprinting is essential for mammalian development. Recent studies have revealed that maternal histone H3 lysine 27 tri-methylation (H3K27me3) can mediate DNA methylation-independent genomic imprinting. However, the regulatory mechanisms and functions of this new imprinting mechanism are largely unknown. Here we demonstrate that maternal Eed, an essential component of the Polycomb group complex 2 (PRC2), is required for establishing H3K27me3 imprinting. We found that all H3K27me3 imprinted genes, including Xist, lose their imprinted expression in Eed maternal KO (matKO) embryos, resulting in male-biased lethality. Surprisingly, although maternal X chromosome inactivation (XmCI) occurs in Eed matKO embryos at preimplantation due to loss of Xist imprinting, it is resolved at peri-implantation. Ultimately, both X chromosomes are reactivated in the embryonic cell lineage prior to random XCI, and only a single X chromosome undergoes random XCI in the extra-embryonic cell lineage. Thus, our study not only demonstrates an essential role of Eed in H3K27me3 imprinting establishment but also reveals a unique XCI dynamics in the absence of Xist imprinting.

2018-11-26 | GSE116713 | GEO

Transcriptional repression by non-canonical EED stimulation of histone deacetylase activity is required for heart maturation independently of H3K27me3 [Microarray]

Project description:Through H3K27me3 and H3K27ac ChIP-seq and microarray data in wile-tpye (WT) and EED-knockout (CKO) mouse cardiomyocytes, we unexpectedly uncovered a novel mechanism of PRC2-mediated gene repression. EED inactivation in the postnatal heart (EEDCKO) caused progressive, lethal dilated cardiomyopathy, with upregulation of components of the slow-twitch muscle gene program. Surprisingly, upregulation of these genes was not associated with their loss of H3K27me3, but rather with their gain of H3K27 acetylation (H3K27ac), an activating histone mark4,5. Moreover, re-expression of EED in juvenile hearts rescued heart function and normalized H3K27ac, but not H3K27me3.

2017-04-14 | GSE73677 | GEO

Transcriptional repression by non-canonical EED stimulation of histone deacetylase activity is required for heart maturation independently of H3K27me3 [RNA-seq]

Project description:Through H3K27me3 and H3K27ac ChIP-seq and microarray data in wile-tpye (WT) and EED-knockout (CKO) mouse cardiomyocytes, we unexpectedly uncovered a novel mechanism of PRC2-mediated gene repression. EED inactivation in the postnatal heart (EEDCKO) caused progressive, lethal dilated cardiomyopathy, with upregulation of components of the slow-twitch muscle gene program. Surprisingly, upregulation of these genes was not associated with their loss of H3K27me3, but rather with their gain of H3K27 acetylation (H3K27ac), an activating histone mark. Moreover, re-expression of EED in juvenile hearts rescued heart function and normalized H3K27ac, but not H3K27me3.

2017-04-14 | GSE86868 | GEO

Transcriptional repression by non-canonical EED stimulation of histone deacetylase activity is required for heart maturation independently of H3K27me3 [ChIP-seq]

Project description:Through H3K27me3 and H3K27ac ChIP-seq and microarray data in wile-tpye (WT) and EED-knockout (CKO) mouse cardiomyocytes, we unexpectedly uncovered a novel mechanism of PRC2-mediated gene repression. EED inactivation in the postnatal heart (EEDCKO) caused progressive, lethal dilated cardiomyopathy, with upregulation of components of the slow-twitch muscle gene program. Surprisingly, upregulation of these genes was not associated with their loss of H3K27me3, but rather with their gain of H3K27 acetylation (H3K27ac), an activating histone mark. Moreover, re-expression of EED in juvenile hearts rescued heart function and normalized H3K27ac, but not H3K27me3.

2017-04-14 | GSE73769 | GEO

The Central Role of EED in the Orchestration of Polycomb Group Complexes

Project description:Polycomb Repressive Complexes 1 and 2 (PRC1 and 2) play a critical role in the epigenetic regulation of transcription during cellular differentiation, stem cell pluripotency, and neoplastic progression1-3. Here we show that the Polycomb group protein EED, a core component of PRC2, physically interacts with and functions as part of the PRC1 complex. Components of PRC1 and PRC2 compete for EED binding. EED functions to recruit PRC1 to H3K27me3 loci and enhances PRC1 mediated H2A ubiquitin E3 ligase activity. Taken together, we uncover the integral role of EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2. EED, uH2A, RING1A, RING1B, BMI1 and H3K27Me3 ChIP-seq in EED stable knockdown and control Scramble DU145 prostate cancer cell line

2014-01-23 | E-GEOD-42566 | biostudies-arrayexpress

Next-generation sequencing Facilitates Quantitative Analysis of Wild Type and EED-/- mice cerebellum Transcriptomes and Genome-wide maps of chromatin state in Wild Type and EED-/- mice cerebellum

Project description:Purpose: The goals of this study are to compare Wild Type and EED-/- cerebellum transcriptome profiling (RNA-seq) to quantitative reverse transcription polymerase chain reaction (qRT–PCR) differentially expressed genes and find target genes. We performed chromatin-immunoprecipitation coupled to sequencing (ChIP-seq) to dissect the relationship between the differentially expressed genes and the occupancy of H3K27me3, H3K27ac and EED. Methods: Cerebellum mRNA profiles of 14-day-old(P14) wild-type (WT) and Embryonic Ectoderm Development conditional knockout (EED-/-) mice were generated by deep sequencing, in triplicate,using Illumina HiSeq 2500 system.All RNA-Seq data were aligned to mouse genome version mm10 using Salmon (v.1.1.0) .We use cluster software and Euclidean distance matrix for the hierarchical clustering analysis of the expressed gene and sample program at the same time, the clustering results can be viewed with javaTreeview. qRT–PCR validation was performed using SYBR Green assays. we performed ChIP-seq using freshly isolated P14 from Wild Type and EED-/- cerebellar tissues . DNA libraries generated from ChIP-DNA and input-DNA were deep-sequenced using HiSeq single-end 50bp. Results:Only transcripts that showed more than 1.5-fold differential expression compared to control were subjected to relevance network analysis. 3149 candidate genes that were differentially expressed with biological functional groups as compared between WT and EED-/- mice .We found that the enrichment of H3K27me3 was decreased H3K27ac was highly increased in EED-/- mice. Conclusions: Our study represents the first detailed analysis of Wild Type and EED-/ mice cerebellum transcriptomes, with three biologic replicates, generated by RNA-seq technology. We report the application of ChIP-sequencing technology for high-throughput profiling of histone modifications in cerebellar cells.

2024-04-02 | GSE169312 | GEO

Polycomb protein EED is required for selective silencing of pluripotency genes upon ESC differentiation

Project description:Eed (embryonic ectoderm development) is a core component of the Polycomb Repressive Complex 2 (PRC2) which catalyzes the methylation of histone H3 lysine 27 (H3K27). Trimethylated H3K27 (H3K27me3) can act as a signal for PRC1 recruitment in the process of gene silencing and chromatin condensation. Previous studies with Eed KO ESCs revealed a failure to down-regulate a limited list of pluripotency factors in differentiating ESCs. Our aim was to analyze the consequences of Eed KO for ESC differentiation. To this end we first analyzed ESC differentiation in the absence of Eed and employed in silico data to assess pluripotency gene expression and H3K27me3 patterns. We linked these data to expression analyses of wildtype and Eed KO ESCs. We observed that in wildtype ESCs a subset of pluripotency genes including Oct4, Nanog, Sox2 and Oct4 target genes progressively gain H3K27me3 during differentiation. These genes remain expressed in differentiating Eed KO ESCs. This suggests that the deregulation of a limited set of pluripotency factors impedes ESC differentiation. Global analyses of H3K27me3 and Oct4 ChIP-seq data indicate that in ESCs the binding of Oct4 to promoter regions is not a general predictor for PRC2-mediated silencing during differentiation. However, motif analyses suggest a binding of Oct4 together with Sox2 and Nanog at promoters of genes that are PRC2-dependently silenced during differentiation. In summary, our data further characterize Eed function in ESCs by showing that Eed/PRC2 is essential for the onset of ESC differentiation. RNAs obtained from undifferentiated (d0) wild type and Eed KO ESCs and from day 3 (d3) and day 7 (d7) respective Ebs were subjected to Affymetrix Mouse Gene 1.0 ST Array. 24 samples in total.

2014-08-28 | E-GEOD-49305 | biostudies-arrayexpress

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