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Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [ChIP-seq]

ABSTRACT: We report the genomic binding profile of KLF5, NANOG and H3K27ac in human naïve ESCs

ORGANISM(S): Homo sapiens

PROVIDER: GSE169673 | GEO | 2022/08/27

REPOSITORIES: GEO

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Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [CUT&Tag]

Project description:Genomic profiling of NANOG binding in KLF4 KLF5 double knockouts naïve human embryonic stem cells

2022-08-27 | GSE190882 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [RNA-seq]

Project description:Transcriptome profiling for KLF4 and/or KLF5 knockout lines in human naïve embryonic stem cells Transcriptome profiling for CRISPRa-LTR7Y or KLF5 overexpression in primed human embryonic stem cells

2022-08-27 | GSE169675 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [ATAC-seq]

Project description:ATAC-seq profiling and comparison for chromatin accessibility in human primed embryonic stem cells (ESCs), primed ESCs overexpressing KLF5, and naïve ESCs.

2022-08-27 | GSE169671 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency

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

2022-08-27 | GSE169678 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [scRNA-seq]

Project description:Single cell transcriptome profiling of human naïve embryonic stem cells.

2022-08-27 | GSE207431 | GEO

Nanog regulates Pou3f1 expression at the exit from pluripotency during gastrulation

Project description:Pluripotency is regulated by a network of transcription factors that maintains early embryonic cells in an undifferentiated state while allowing them to proliferate. NANOG is a critical factor for maintaining pluripotency and its role in primordial germ cell differentiation has been well described. However, Nanog is expressed during gastrulation across all the posterior epiblast, and only later in development its expression is restricted to primordial germ cells. In this work, we unveiled a previously unknown mechanism by which Nanog specifically represses genes involved in anterior epiblast lineage. Analysis of transcriptional data from both embryonic stem cells and gastrulating mouse embryos revealed Pou3f1 expression to be negatively correlated with that of Nanog during the early stages of differentiation. We have functionally demonstrated Pou3f1 to be a direct target of NANOG by using a dual transgene system for the controlled expression of Nanog. Use of Nanog null ES cells further demonstrated a role for Nanog in repressing a subset of anterior neural genes. Deletion of a NANOG binding site (BS) located nine kilobases downstream of the transcription start site of Pou3f1 revealed this BS to have a specific role in the regionalization of the expression of this gene in the embryo. Our results indicate an active role of Nanog inhibiting neural regulatory networks by repressing Pou3f1 at the onset of gastrulation.

2019-10-31 | GSE138818 | GEO

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

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. We analysed two technical replicates of each cell line.

2014-01-06 | E-GEOD-53529 | biostudies-arrayexpress

The pluripotency factor NANOG controls primitive hematopoiesis and directly regulates Tal1.

Project description:Progenitors of the first hematopoietic cells in the mouse arise in the early embryo from Brachyury-positive multipotent cells in the posterior-proximal region of the epiblast, but the mechanisms that specify primitive blood cells are still largely unknown. Pluripotency factors maintain uncommitted cells of the blastocyst and embryonic stem cells in the pluripotent state. However, little is known about the role played by these factors during later development, despite their being expressed in the postimplantation epiblast. Using a dual transgene system for controlled expression at postimplantation stages, we found that Nanog blocks primitive hematopoiesis in the gastrulating embryo, resulting in a loss of red blood cells and downregulation of erythropoietic genes. Accordingly, Nanog deficient embryonic stem cells are prone to erythropoietic differentiation. Moreover, Nanog expression in adults prevents the maturation of erythroid cells. By analysis of previous data for NANOG binding during stem cell differentiation and CRISPR/Cas9 genome editing, we found that Tal1 is a direct NANOG target. Our results show that Nanog regulates primitive hematopoiesis by directly repressing critical erythroid lineage specifiers.

2019-02-20 | GSE119467 | GEO

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

2014-01-06 | GSE53529 | GEO