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The role of Phc1 in organizing the chromatin interactions of the Nanog locus in ESCs

ABSTRACT: The role of Phc1 in organizing the chromatin interactions of the Nanog locus in ESCs

PROVIDER: PRJNA649985 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12363400_1.fastq.gz	Fastqsanger.gz
	SRR12363400_2.fastq.gz	Fastqsanger.gz
	SRR12363401_1.fastq.gz	Fastqsanger.gz
	SRR12363401_2.fastq.gz	Fastqsanger.gz
	SRR12363402_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The role of Phc1 in organizing the chromatin interactions of the Nanog locus in ESCs

Project description:To look into whether Phc1 is involved in organizing the chromatin interactions of the Nanog locus in ESCs. We performed circularized chromosome conformation capture sequencing (4C-seq) of the genome-wide regions interacting with the Nanog locus in both Phc1+/+ and Phc1-/- mESCs. By doing so, we showed that ablation of Phc1 impaired the genome-wide chromatin interactions of the Nanog locus in mESCs.

2021-03-02 | GSE155524 | GEO

Analysis of chromatin interactions to define the HoxB landscape in ESCs and mouse embryos

Project description:The goal is to examine the interactions at chromatin level between two specific Oct4/Nanog binding-sites in the vicinity of Hoxb1 in ESCs and E9.5 mouse embryos.

2020-01-01 | GSE94953 | GEO

PHC1 maintains pluripotency by organizing genome-wide chromatin interactions of the Nanog locus.

Project description:Polycomb group (PcG) proteins maintain cell identity by repressing gene expression during development. Surprisingly, emerging studies have recently reported that a number of PcG proteins directly activate gene expression during cell fate determination process. However, the mechanisms by which they direct gene activation in pluripotency remain poorly understood. Here, we show that Phc1, a subunit of canonical polycomb repressive complex 1 (cPRC1), can exert its function in pluripotency maintenance via a PRC1-independent activation of Nanog. Ablation of Phc1 reduces the expression of Nanog and overexpression of Nanog partially rescues impaired pluripotency caused by Phc1 depletion. We find that Phc1 interacts with Nanog and activates Nanog transcription by stabilizing the genome-wide chromatin interactions of the Nanog locus. This adds to the already known canonical function of PRC1 in pluripotency maintenance via a PRC1-dependent repression of differentiation genes. Overall, our study reveals a function of Phc1 to activate Nanog transcription through regulating chromatin architecture and proposes a paradigm for PcG proteins to maintain pluripotency.

| S-EPMC8121881 | biostudies-literature

TINC - a method to dissect transcriptional complexes at single locus resolution - reveals novel Nanog regulators in mouse embryonic stem cells

Project description:Cellular identity is ultimately dictated by the interaction of transcription factors with regulatory elements (REs) to control gene expression. Advances in genome-wide epigenome profiling techniques have significantly increased our understanding of cell-specific utilization of REs. However, it remains difficult to dissect the majority of factors that interact with these REs due to the lack of appropriate techniques. To address this issue, we developed a novel epigenetic method termed TINC: TALE-mediated Isolation of Nuclear Chromatin. Using TINC we interrogated the protein complex formed at the Nanog promoter in embryonic stem cells (ESCs) and identified many known interactors as well as numerous previously unknown complex members, including RCOR2. Further interrogation of the role of RCOR2 in the ESC network revealed its involvement in the repression of lineage genes and the fine-tuning of pluripotency genes. Consequently, using the Nanog promoter as a paradigm, we demonstrated the power of TINC to provide important insights into the molecular makeup of transcriptional complexes at individual REs as well as into control of cellular identity in general.

2020-12-14 | PXD022088 | Pride

Reprogramming by Sall4, Nanog, Esrrb and Lin28 produces high quality iPSCs with a molecular signature of developmental potency that resembles ESCs.

Project description:To reveal a gene expression signature associated with developmental competence, we selected the following groups of iPSC lines for microarray analysis. i) “Poor quality” iPSCs: This group included the three OSKM-iPSC lines Nanog-GFP OSKM#2, Oct4-GFP OSKM#2 and KH2 OSKM27, that either did not produce fully developed pups or produced very low number of pups; ii) “Good quality” iPSCs: This group included BC_2 OSKM28 and Nanog-GFP SNEL#3, both of which gave rise to live, normal pups that survived only few hours; iii) “High quality” iPSCs consisting of Nanog-GFP SNEL#2 and Oct4-GFP SNEL#1, both of which generated live pups that survived postnatally (representative pups from each iPSC group are shown in Figure S5). iv) As controls we used Nanog-GFP, Oct4-GFP and KH229 ESCs.

2014-09-08 | GSE45173 | GEO

BACH1 Recruits NANOG and Histone H3 Lysine 4 Methyltransferase MLL/SET1 Complexes to Regulate Enhancer-promoter Activity and Maintains Pluripotency

Project description:Maintenance of stem-cell identity requires proper regulation of enhancer activity. Both transcription factors OCT4/SOX2/NANOG and histone methyltransferase complexes MLL/SET1 were shown to regulate enhancer activity, but how they are regulated in embryonic stem cells (ESCs) remains further studies. Here, we report a transcription factor BACH1, who which directly interacts with OCT4/SOX2/NANOG (OSN) and MLL/SET1 methyltransferase complexes and maintains pluripotency in mouse ESCs (mESCs). BTB domain and bZIP domain of BACH1 are required for these interactions and pluripotency maintenance. Loss of BACH1 reduced the interaction between NANOG and MLL1/SET1 complexes, and decreased their occupancy on chromatin, and further decreased H3 lysine 4 trimethylation (H3K4me3) level on gene promoters and (super-) enhancers, leading to decreased enhancer activity and transcription activity, especially on stemness-related genes. Moreover, BACH1 recruited NANOG through chromatin looping and regulated remote NANOG binding, fine-tuning enhancer-promoter activity and gene expression. Collectively, these observations suggest that BACH1 maintains pluripotency in ESCs by recruiting NANOG and MLL/SET1 complexes to chromatin and maintaining the trimethylated state of H3K4 and enhancer-promoter activity, especially on stemness-related genes.

2021-01-12 | GSE142519 | GEO

Reprogramming by Sall4, Nanog, Esrrb and Lin28 produces high quality iPSCs with a molecular signature of developmental potency that resembles ESCs.

2014-09-08 | E-GEOD-45173 | biostudies-arrayexpress

NANOG amplifies STAT3 activation and they synergistically induce the naïve pluripotent program

Project description:We generated Nanog-/- iPSCs from both EpiSCs and pre-iPSCs. We wanted to compare the global gene expression profile of these iPSCs to their parental cells lines and to wild-type and Nanog-/- ESCs.

2014-01-06 | GSE53529 | GEO

TINC - a method to dissect transcriptional complexes at single locus resolution - reveals novel Nanog regulators in mouse embryonic stem cells

Project description:We developed a novel epigenetic method termed TINC: TALE-mediated Isolation of Nuclear Chromatin. Using TINC we interrogated the protein complex formed at the Nanog promoter in embryonic stem cells (ESCs) and identified many known interactors as well as numerous previously unknown complex members, including RCOR2. Further interrogation of the role of RCOR2 in the ESC network revealed its involvement in the repression of lineage genes and the fine-tuning of pluripotency genes. Consequently, using the Nanog promoter as a paradigm, we demonstrated the power of TINC to provide important insights into the molecular makeup of transcriptional complexes at individual REs as well as into control of cellular identity in general.

2020-11-05 | GSE160816 | GEO

Analysis of genes differentially expressed depending on Oct4/Nanog induction and of chromatin interactions to define the HoxB landscape in ESCs and mouse embryos

Project description:Analysis of genes differentially expressed depending on Oct4/Nanog induction and of chromatin interactions to define the HoxB landscape in ESCs and mouse embryos

| PRJNA374895 | ENA

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