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Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [ATAC-Seq]

ABSTRACT: Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [ATAC-Seq]

PROVIDER: PRJNA454458 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7088936_1.fastq.gz	Fastqsanger.gz
	SRR7088936_2.fastq.gz	Fastqsanger.gz
	SRR7088937_1.fastq.gz	Fastqsanger.gz
	SRR7088937_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [RNA-Seq]

Project description:Embryonic stem cells (ESCs) maintain pluripotency through unique epigenetic states. When ESCs commit to a specific cell lineage, changes in histone modifications and DNA methylation accompany the transition to more specialized cell types. Investigating how epigenetic regulation maintains pluripotency is a critical component in order to generate the required cell types for future clinical application. Uhrf1 is a widely known hemi-methylated DNA binding protein, playing a role in heterochromatin formation alongside G9a, Trim28 and HDACs. In addition, it has been demonstrated that Uhrf1 functions to maintain DNA methylation through the recruitment of Dnmt1. Although Uhrf1 is not essential in ESC self-renewal, it still remains elusive how Uhrf1 regulates pluripotency. Here, we set out to elucidate the role of Uhrf1 in pluripotent stem cells. We found that Uhrf1 forms a complex with the active trithorax group of transcriptional regulators, in particular the Setd1a/COMPASS complex. Our data show that loss of Uhrf1 causes a dramatic reduction of bivalent histone marks, in particular those associated with neuroectoderm and mesoderm specification. Overall, our data demonstrate that Uhrf1 safeguards the balance between pluripotency and differentiation via the Setd1a/COMPASSS complex, through which Uhrf1 mediates bivalent histone modifications.

2018-05-02 | GSE113914 | GEO

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [ChIP-Seq]

2018-05-02 | GSE113913 | GEO

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [ATAC-Seq]

2018-05-02 | GSE113912 | GEO

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a

Project description:Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a

| PRJNA454457 | ENA

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [RNA-Seq]

Project description:Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [RNA-Seq]

| PRJNA454459 | ENA

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [ChIP-Seq]

Project description:Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a [ChIP-Seq]

| PRJNA454460 | ENA

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a.

Project description:Embryonic stem cells (ESCs) maintain pluripotency through unique epigenetic states. When ESCs commit to a specific lineage, epigenetic changes in histones and DNA accompany the transition to specialized cell types. Investigating how epigenetic regulation controls lineage specification is critical in order to generate the required cell types for clinical applications. Uhrf1 is a widely known hemi-methylated DNA-binding protein, playing a role in DNA methylation through the recruitment of Dnmt1 and in heterochromatin formation alongside G9a, Trim28, and HDACs. Although Uhrf1 is not essential in ESC self-renewal, it remains elusive how Uhrf1 regulates cell specification. Here we report that Uhrf1 forms a complex with the active trithorax group, the Setd1a/COMPASS complex, to maintain bivalent histone marks, particularly those associated with neuroectoderm and mesoderm specification. Overall, our data demonstrate that Uhrf1 safeguards proper differentiation via bivalent histone modifications.

| S-EPMC6030064 | biostudies-literature

SCML2 establishes germline-specific bivalent domains.

Project description:Bivalent domains marked with repressive H3K27me3 and activating H3K4me2/3 are a molecular signature of totipotency in stem cells and development. While bivalent domains are retained throughout the germline to recover totipotency in the next generation, the mechanisms establishing bivalent domains remains unknown. Here we demonstrate that a germline-specific Polycomb protein, SCML2, binds to chromatin containing hypomethylated DNA to induce H3K27me3, thereby initiating the establishment of germline-specific bivalent domains in mice. SCML2 regulates two distinct classes of autosomal bivalent domains, the first are maintained constitutively through spermatogenesis (Class I), and the second are specifically established during meiosis (Class II). In postmeiotic spermatids, the loss of H3K27me3 leads to an increase of H3K4me2/3 on bivalent domains and disorganization of pericentromic heterochromatin. We propose that SCML2 regulates dynamic bivalent domains in the germline as a molecular imprint to recover totipotency after fertilization.

2018-04-12 | GSE89502 | GEO

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-05-02 | GSE113915 | GEO

Bivalent Chromatin Marks Developmental Regulatory Genes in the Mouse Embryonic Germline in Vivo

Project description:We developed a ChIP protocol for the analysis of histone marks using less than 10,000 cells per IP, and used it to investigate the chromatin state of E11.5 mouse primordial germ cells (PGCs). A genome-wide ChIP-Seq analysis of E11.5 PGCs revealed a distribution of H3K4me3/H3K27me3 bivalent domains highly enriched for developmental regulatory genes. H3K4me3 and H3K27me3 ChIP-Seq from mouse E11.5 primordial germ cells.

2013-05-30 | E-GEOD-46396 | biostudies-arrayexpress

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