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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE169678 | 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 [scRNA-seq]

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

2022-08-27 | GSE207431 | GEO

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

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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 [ChIP-seq]

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

2022-08-27 | GSE169673 | 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

The SIN3A/HDAC Corepressor Complex Functionally Cooperates with NANOG to Promote Pluripotency.

Project description:Although SIN3A is required for the survival of early embryos and embryonic stem cells (ESCs), the role of SIN3A in the maintenance and establishment of pluripotency remains unclear. Here, we find that the SIN3A/HDAC corepressor complex maintains ESC pluripotency and promotes the generation of induced pluripotent stem cells (iPSCs). Members of the SIN3A/HDAC corepressor complex are enriched in an extended NANOG interactome and function in transcriptional coactivation in ESCs. We also identified a critical role for SIN3A and HDAC2 in efficient reprogramming of somatic cells. Mechanistically, NANOG and SIN3A co-occupy transcriptionally active pluripotency genes in ESCs and also co-localize extensively at their genome-wide targets in pre-iPSCs. Additionally, both factors are required to directly induce a synergistic transcriptional program wherein pluripotency genes are activated and reprogramming barrier genes are repressed. Our findings indicate a transcriptional regulatory role for a major HDAC-containing complex in promoting pluripotency.

| S-EPMC5328122 | biostudies-literature

NaNog: A pluripotency homeobox (master) molecule.

Project description:One of the most intriguing aspects of cell biology is the state of pluripotency, where the cell is capable of self-renewal for as many times as deemed "necessary", then at a specified time can differentiate into any type of cell. This fundamental process is required during organogenesis in foetal life and importantly during tissue repair in health and disease. Pluripotency is very tightly regulated, as any dysregulation can result in congenital defects, inability to repair damage, or cancer. Fuelled by the relatively recent interest in stem cell biology and tissue regeneration, the molecules implicated in regulating pluripotency have been the subject of extensive research. One of the important molecules involved in pluripotency, is NaNog, the subject of this article.

| S-EPMC4625207 | biostudies-literature

Nanog, Oct4 and Tet1 interplay in establishing pluripotency.

Project description:A few central transcription factors inside mouse embryonic stem (ES) cells and induced pluripotent stem (iPS) cells are believed to control the cells' pluripotency. Characterizations of pluripotent state were put forward on both transcription factor and epigenetic levels. Whereas core players have been identified, it is desirable to map out gene regulatory networks which govern the reprogramming of somatic cells as well as the early developmental decisions. Here we propose a multiple level model where the regulatory network of Oct4, Nanog and Tet1 includes positive feedback loops involving DNA-demethylation around the promoters of Oct4 and Tet1. We put forward a mechanistic understanding of the regulatory dynamics which account for i) Oct4 overexpression is sufficient to induce pluripotency in somatic cell types expressing the other Yamanaka reprogramming factors endogenously; ii) Tet1 can replace Oct4 in reprogramming cocktail; iii) Nanog is not necessary for reprogramming however its over-expression leads to enhanced self-renewal; iv) DNA methylation is the key to the regulation of pluripotency genes; v) Lif withdrawal leads to loss of pluripotency. Overall, our paper proposes a novel framework combining transcription regulation with DNA methylation modifications which, takes into account the multi-layer nature of regulatory mechanisms governing pluripotency acquisition through reprogramming.

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Activin/Nodal signalling maintains pluripotency by controlling Nanog expression.

Project description:The pluripotent status of embryonic stem cells (ESCs) confers upon them the capacity to differentiate into the three primary germ layers, ectoderm, mesoderm and endoderm, from which all the cells of the adult body are derived. An understanding of the mechanisms controlling pluripotency is thus essential for driving the differentiation of human pluripotent cells into cell types useful for clinical applications. The Activin/Nodal signalling pathway is necessary to maintain pluripotency in human ESCs and in mouse epiblast stem cells (EpiSCs), but the molecular mechanisms by which it achieves this effect remain obscure. Here, we demonstrate that Activin/Nodal signalling controls expression of the key pluripotency factor Nanog in human ESCs and in mouse EpiSCs. Nanog in turn prevents neuroectoderm differentiation induced by FGF signalling and limits the transcriptional activity of the Smad2/3 cascade, blocking progression along the endoderm lineage. This negative-feedback loop imposes stasis in neuroectoderm and mesendoderm differentiation, thereby maintaining the pluripotent status of human ESCs and mouse EpiSCs.

| S-EPMC2687465 | biostudies-literature

SRSF3 promotes pluripotency through Nanog mRNA export and coordination of the pluripotency gene expression program.

Project description:The establishment and maintenance of pluripotency depend on precise coordination of gene expression. We establish serine-arginine-rich splicing factor 3 (SRSF3) as an essential regulator of RNAs encoding key components of the mouse pluripotency circuitry, SRSF3 ablation resulting in the loss of pluripotency and its overexpression enhancing reprogramming. Strikingly, SRSF3 binds to the core pluripotency transcription factor Nanog mRNA to facilitate its nucleo-cytoplasmic export independent of splicing. In the absence of SRSF3 binding, Nanog mRNA is sequestered in the nucleus and protein levels are severely downregulated. Moreover, SRSF3 controls the alternative splicing of the export factor Nxf1 and RNA regulators with established roles in pluripotency, and the steady-state levels of mRNAs encoding chromatin modifiers. Our investigation links molecular events to cellular functions by demonstrating how SRSF3 regulates the pluripotency genes and uncovers SRSF3-RNA interactions as a critical means to coordinate gene expression during reprogramming, stem cell self-renewal and early development.

| S-EPMC5963917 | biostudies-literature

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