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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE160816 | GEO | 2020/11/05

REPOSITORIES: GEO

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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

Nanog CAPTURE LC/MS/MS_University of Tsukuba

Project description:Identification of Nanog promoter binding protein by CAPTURE

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The pluripotency factor NANOG regulates the mitotic program of adult stratified epithelia.

Project description:NANOG is a key transcription factor for pluripotency in embryonic stem cells. However, its role in adult tissues remains largely unexplored. Here, we show that mouse NANOG is expressed in the progenitor layer of stratified epithelia, including esophagus, forestomach and skin. Accordingly, the Nanog promoter is hypomethylated in the epithelial layers of the esophagus and forestomach. Interestingly, ubiquitous transgenic overexpression of NANOG in mice induces hyperplasia in stratified epithelia, but not in other tissues. Mechanistically, we show that NANOG transcriptionally activates the mitotic program selectively in stratified epithelia, and endogenous NANOG directly binds the Aurora kinase A (Aurka) promoter in keratinocytes. Finally, human and mouse squamous cell carcinomas (SCCs) express NANOG and its levels positively correlate with those of AURKA in human head and neck SCCs. Together, these results implicate a lineage-restricted mitogenic role of NANOG in normal stratified epithelia and its derived carcinomas.

2014-06-27 | GSE48370 | GEO

Pou5f3, SoxB1 and Nanog remodel chromatin on High Nucleosome Affinity Regions at Zygotic Genome Activation.

Project description:Purpose: Find out the consequences of Pou5f3/Oct4 and Nanog binding to the nucleosome distribution before and after Zygotic Genome Activation Methods: MNase-seq of the wild-type(WT), Pou5f3 (MZspg) and Nanog (MZnanog) mutant zebrafish embryos at 512-cell stage and dome stage. Results: Nanog, Sox19b and Pou5f3 bind to the High Nucleosome Affinity Regions (HNARs). HNARs are spanning over 600 bp, featuring high in vivo and predicted in vitro nucleosome occupancy and high predicted propeller twist DNA shape value. We suggest a two-step model, where the same intrinsic DNA properties of HNAR promote both high nucleosome occupancy and differential binding of TFs. In the first step, already prior to ZGA, Pou5f3 and Nanog reduce nucleosome occupancy on HNARs genome-wide. In the second step, Nanog and Pou5f3/SoxB1 complex maintain open chromatin state on the subset of HNARs, acting synergistically. Nanog binds to the HNAR center, while the Pou5f3/SoxB1 complex stabilizes the flanks.

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Gene expression signatures for Nanog-positive and Nanog-negative hepatocellular carcinoma cells

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Nanog-induced intestinal and colonic hyperplasia

Project description:Though expression of the homeobox transcription factor Nanog is generally restricted to pluripotent cells and early germ cells, recent reports have found that Nanog is re-expressed in somatic and germ cell tumors associated with poor differentiation and aggressive disease progression. To elucidate its oncogenic properties, a modified Tet-On system was utilised to generate Nanog-inducible mice. By dexamethasone and doxycycline injection, similar Nanog expression levels as in wild-type embryonic stem cells were obtained in all major organs except for brain. Ectopic Nanog expression resulted in intestinal and colonic epithelium hyperplasia-intestinal villi had doubled in length and hyperplastic epithelium outgrowths were seen after 7 days. The tumor suppressor gene Cdx2 was downregulated at onset of Nanog expression, suggesting that crosstalk between Nanog and Cdx2 is conserved from early embryo development to adulthood. Although the mice died before they could form tumors, Cdx2 repression and intestinal hyperplasia links Nanog to tumor initiation.

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Nanog-induced intestinal and colonic hyperplasia

2014-08-11 | E-GEOD-31413 | biostudies-arrayexpress

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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

Two super-enhancers regulate Nanog expression through distinct mechanisms [45del]

Project description:Enhancers are critical regulators of gene expression which are historically defined using plasmid-based approaches. Recent work has emphasized that enhancers operate by alleviating promoter-proximal pause release, implying that a single enhancer operates on a gene at any given moment. By contrast, our previous work postulated that two super-enhancers (SEs) may simultaneously operate on a single gene. To address this discrepancy we employed genomic editing, single cell analyses, and genome-wide approaches to assess how two SEs regulate Nanog expression in embryonic stem cells. We first demonstrate both distance and orientation independence in native chromatin, eliminating the issues raised with plasmid-based approaches. We also demonstrate that two SEs simultaneously operate on Nanog by regulating different phases of transcription, with one SE operating by recruiting and/or initiating RNA Polymerase II, and the second promoting transcriptional elongation after promoter-proximal pause release. These findings imply SEs can use different mechanisms to regulate expression.

2021-01-10 | GSE143960 | GEO

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