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A cytokine screen using CRISPR-Cas9 knock-in reporter pig iPS cells reveals that Activin A regulates NANOG

ABSTRACT: NANOG functions as the gateway for the generation of pluripotent stem cells (PSCs) in mice and humans. NANOG protein is highly expressed in pig pre-implantation embryos, indicating NANOG is a conserved pluripotency-associated factor. However, pig NANOG reporter PSCs have yet to be established, and the regulation of pluripotency by NANOG is not completely understood in this animal. In this study, pig NANOG tdTomato knock-in reporter PSCs were established using CRISPR/Cas9. The resulting cell line was treated with several cytokines and inhibitors to identify the key pathway that regulates NANOG expression and the development of pluripotency.

ORGANISM(S): Sus scrofa

PROVIDER: GSE141935 | GEO | 2019/12/13

REPOSITORIES: GEO

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A cytokine screen using CRISPR-Cas9 knock-in reporter pig iPS cells reveals that Activin A regulates NANOG

Project description:A cytokine screen using CRISPR-Cas9 knock-in reporter pig iPS cells reveals that Activin A regulates NANOG

| PRJNA595349 | ENA

Nanog Independent Reprogramming to iPSCs with Canonical Factors

Project description:It has been suggested that the transcription factor Nanog is essential for the establishment of pluripotency during the derivation of embryonic stem (ES) cells and induced pluripotent stem (iPS) cells. However, successful reprogramming to pluripotency with a growing list of divergent transcription factors, at ever increasing efficiencies, suggests that there may be many distinct routes to a pluripotent state. Here, we have investigated whether Nanog is necessary for reprogramming murine fibroblasts under highly efficient conditions using the canonical reprogramming factors Oct4, Sox2, Klf4 and cMyc. In agreement with prior results, the efficiency of reprogramming Nanog-/- fibroblasts was significantly lower than that of control fibroblasts. However, in contrast to previous findings, we were able to reproducibly generate iPS cells from Nanog-/- fibroblasts that effectively contributed to chimeric mice. Thus while Nanog may be an important mediator of reprogramming it is not required for establishing pluripotency in the mouse, even under standard conditions. In order to further evaluate the equivalency of Nanog null iPSC to nanog null ESCs, we have performed RNAseq on two independent nanog null iPSC lines, as well as Nanog Null ESC, WT ESC and iPSCs as well as MEFs. As a negativve control for reprogramming we have analyzed a partially reprogrammed iPSC line. 2-4 biological replicates each of 7 conditions (WT MEFs, WT ESC, WT iPSC, WT partially reprogrammed iPSC (piPS), Nanog null ESC, Nanog null iPSC clone G2 and Nanog null iPSC clone G5)

2014-01-01 | E-GEOD-53212 | biostudies-arrayexpress

Nanog Independent Reprogramming to iPSCs with Canonical Factors

2014-01-01 | GSE53212 | GEO

NANOG prion-like assembly mediates DNA bridging

Project description:NANOG is a key stem cell pluripotency factor. NANOG’s unique ability to form prion-like assemblies provides a cooperative and concerted DNA bridging mechanism essential for chromatin reorganization and dose-sensitive activation of ground state pluripotency. We take advantage of Hi-C and ChIP-seq experiments to directly address whether NANOG can bridge DNA elements together in human cells, and our results support this.

2022-02-15 | GSE190567 | GEO

Transcriptional profiles by deep sequencing (RNA-seq) of papillomas generated using the DMBA/TPA protocol from control and transgenic Nanog overexpressing mice

Project description:NANOG is a key pluripotency factor in embryonic stem cells that is frequently expressed in squamous cell carcinomas (SCCs). However, a direct link between NANOG and SCCs remains to be established. Here, we show that inducible overexpression of NANOG in mouse skin epithelia dramatically promotes the formation of carcinomas upon chemical carcinogenesis. Gene expression analyses in pre-malignant skin indicate that NANOG induces a large set of genes associated to stemness and to epithelial-mesenchymal transition (EMT).

2016-05-25 | GSE56566 | GEO

The Sin3a/HDAC co-repressor complex cooperates with Nanog in promoting stem cell pluripotency and somatic cell reprogramming [ChIP-Seq]

Project description:Despite the requirement of Sin3a for survival of early embryos and embryonic stem cells (ESCs), mechanistic action of Sin3a in the maintenance and establishment of pluripotency remains unexplored. Here we report the transcriptional regulatory roles of Sin3a in maintaining ESC pluripotency and in reprogramming somatic cells towards full pluripotency. Sin3a/HDAC complex members were enriched in an extended Nanog interactome and exhibited a predominant transcriptional co-activator role at a global level in ESCs. We also established a critical role for Sin3a in efficient reprogramming of somatic cells towards full pluripotency. Nanog and Sin3a co-localize at almost all of their genome-wide targets in pre-iPSCs, and both factors are required to directly induce a synergistic transcriptional program wherein pluripotency genes are activated and reprogramming barrier genes are repressed. Our results, for the first time, establish positive roles of the Sin3a/HDAC complex in the maintenance and establishment of pluripotency.

2017-02-21 | GSE91021 | GEO

The Sin3a/HDAC co-repressor complex cooperates with Nanog in promoting stem cell pluripotency and somatic cell reprogramming [Microarray Expression]

2017-02-21 | GSE90986 | GEO

Global gene expression analysis in murine iPS cells derived with mouse and human Nanog orthologs

Project description:Nanog null neural stem (NS) cells were reprogrammed to naive pluripotency in 2i/LIF conditions with mouse (m) Nanog and human (h) Nanog. Global gene expression in resulting iPS cells was compared to embryonic stem (ES) cells and nanog null NS cells.

2011-10-24 | GSE32464 | GEO

Chromatin immunoprecipitation of Tcf3, Oct4 and nanog in mouse embryonic stem cells

Project description:Embryonic stem cells have a unique regulatory circuitry, largely controlled by the transcription factors Oct4, Sox2 and Nanog, which generates a gene expression program necessary for pluripotency and self-renewal (Boyer et al. 2005; Loh et al. 2006; Chambers et al. 2003; Mitsui et al. 2003; Nichols et al. 1998). How external signals connect to this regulatory circuitry to influence embryonic stem cell fate is not known. We report here that a terminal component of the canonical Wnt pathway in embryonic stem cells, the transcription factor Tcf3, co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog. Thus Tcf3 is an integral component of the core regulatory circuitry of ES cells, which includes an autoregulatory loop involving the pluripotency regulators. Both Tcf3 depletion and Wnt pathway activation cause increased expression of Oct4, Nanog and other pluripotency factors and enhance pluripotency and self-renewal. Our results reveal that the Wnt pathway, through Tcf3, brings developmental signals directly to the core regulatory circuitry of ES cells to influence the balance between pluripotency and differentiation.

2008-02-28 | E-TABM-409 | biostudies-arrayexpress

Global gene expression analysis in murine iPS cells derived with mouse, chick and zebrafish Nanog orthologs

Project description:Nanog null neural stem (NS) cells were reprogrammed to naive pluripotency in 2i/LIF conditions with chick (c) and zebrafish (z) Nanog orthologs. Global gene expression was compared to iPS cells derived with mouse (m) Nanog. Murine iPS cells derived with zebrafish nanog, chick nanog, and mouse nanog orthologs (2 replicates each).

2011-10-23 | E-GEOD-32650 | biostudies-arrayexpress

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