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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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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

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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.

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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.

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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.

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

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

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