Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of murine embryonic and epiblast stem cells under IQ1 treatment and Ctnnb1 K49 acetylation conditions

ABSTRACT: Naïve pluripotency represents the ground state of mammalian development, but the molecular mechanisms controlling its establishment remain incompletely defined. To clarify the role of β-catenin (Ctnnb1) acetylation, we performed microarray-based transcriptome profiling of murine embryonic stem cells (ESCs, naïve) and epiblast stem cells (EpiSCs, primed) under different culture conditions. Particular focus was placed on the acetylation of Ctnnb1 at lysine 49 (K49) and its modulation by IQ1, a small molecule that inhibits Ep300 function and enhances K49 acetylation. This dataset enables comparison of gene expression signatures between naïve and primed states and provides insights into the induction of naïve-like characteristics in EpiSCs following IQ1 treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE107889 | GEO | 2017/12/12

SECONDARY ACCESSION(S): PRJNA421878

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling of murine embryonic and epiblast stem cells under IQ1 treatment and Ctnnb1 K49 acetylation conditions

Project description:Gene expression profiling of murine embryonic and epiblast stem cells under IQ1 treatment and Ctnnb1 K49 acetylation conditions

| PRJNA421878 | ENA

Gene expression profile of Epiblast stem cells

Project description:To characterize the EpiSCs (Epiblast stem cells) we established in our lab, we have employed whole genome microarray expression profiling as a platform to distinguish the EpiSCs (primed state) from ES cells (naïve state).

2018-11-30 | GSE75660 | GEO

Formative pluripotent stem cells show features of epiblast cells poised for gastrulation

Project description:The pluripotency of mammalian early and late epiblast could be recapitulated by naïve embryonic stem cells (ESCs) and primed epiblast stem cells (EpiSCs), respectively. However, these two states of pluripotency may not be sufficient to reflect the full complexity and developmental potency of the epiblast during mammalian early development. Here we report the establishment of self-renewing formative pluripotent stem cells (fPSCs) which manifest features of epiblast cells poised for gastrulation. fPSCs can be established from different mouse ESCs, pre-/early-gastrula epiblasts and induced PSCs. Similar to pre-/early-gastrula epiblasts, fPSCs show the transcriptomic features of formative pluripotency, which are distinct from naïve ESCs and primed EpiSCs. fPSCs show the unique epigenetic states of E6.5 epiblast, including the super-bivalency of a large set of developmental genes. Just like epiblast cells immediately before gastrulation, fPSCs can efficiently differentiate into three germ layers and primordial germ cells (PGCs) in vitro. Thus, fPSCs highlight the feasibility of using PSCs to explore the development of mammalian epiblast.

2021-02-19 | GSE154290 | GEO

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [RNA-Seq]

Project description:Epigenetic control of cell type is a critical determinant in cell type stability and permissive differentiation. However, the epigenetic control mechanisms are not well understood. Here, we explore the epigenetic control of the conversion of primed mouse EpiSCs to naïve mouse ESCs as a mimic for early stages of embryonic development. Whilst the conversion of naïve to primed state is relatively permissive and mimics a normal developmental program, the reverse process, primed to naïve is inefficient in the absence of transgenes, which suggests the presence of potent epigenetic barriers that resist this artificial dedifferentiation. Here, we identify the histone acetylation reader BRD8 as a one-way barrier that blocks the conversion of primed to naïve cells. BRD8 works by maintaining histone acetylation on promoters and transcribed gene bodies and it’s absence promotes the formation of heterochromatin.

2024-12-08 | GSE253031 | GEO

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ChIP-Seq]

2024-12-08 | GSE253030 | GEO

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ATAC-Seq]

2024-12-08 | GSE253029 | GEO

The DNA methylome of Epiblast Stem Cells and Embryonic Stem Cells is distinct and not fully reversible

Project description:Embryonic Stem Cells (ESCs) and Epiblast Stem Cells (EpiSCs) are the in vitro representants of naïve and primed pluripotency, respectively. It is currently unclear how their epigenome underpin the phenotypic and molecular characteristics of these states of pluripotency. Here, we performed the first qualitative and quantitative comparison of DNA methylation between ESCs and EpiSCs. The global level and genomic distribution of DNA methylation were very similar between the two cell types. However, the analysis of promoter methylation patterns in EpiSCs revealed several distinct features: (i) the repression of germline-related genes by DNA methylation, a process already ongoing in ESCs but far more pronounced in EpiSCs; (ii) the hypermethylation of promoters (especially CpG rich) in EpiSC compared to both ESCs and dissected epiblasts from E6.5 and E7.5 embryos; (iii) the inability of hypomethylated (Dnmt-deficient) ESCs to be converted into EpiSCs despite their ability to self-renew. Altogether, our data show that DNA methylation is an important epigenetic regulator of gene expression in EpiSCs and suggest that it is essential for the obtention of EpiSCs.

2014-04-28 | GSE47793 | GEO

AMPK activation reverts mouse epiblast stem cells to naïve state

Project description:Reversion from primed to naïve pluripotent status has been achieved by various signaling manipulation, but it is still unclear what signaling is the actual driving force to get over the hurdle from primed to naïve pluripotency. We previously reported that activation of AMP kinase (AMPK) contributed to maintenance of naïve pluripotency. Here, we further show that AMPK activators, AICAR, A769662 or metformin, can induce the reversion of primed mouse epiblast stem cells (mEpiSCs) to naïve pluripotent state. Primed mEpiSCs in our naïve cell culture condition with leukemia inhibitory factor (LIF) and 2 kinase inhibitors (2i) (2iL) never gave rise to naïve state cells. Addition of AICAR alone even in the absence of 2iL or either of AMPK inhibitors with LIF induced appearance of naïve-like cells from primed mEpiSCs. Through maintenance and passages of these cells in 2iL condition, clear naïve-like morphology colonies were purely obtained. They showed core naïve protein expression, and global naïve gene expression profiles. These cells contributed to chimeric mice including germline transmission. Inhibition of p38 signaling abolished the AMPK-elicited reversion and forced activation of p38 in primed mEpiSCs partially reproduced the naïve cell induction, suggesting that p38 is one of the critical downstream in AMPK activation. AMPK pathway should be a novel critical driving force in reversion of primed to naïve pluripotency.

2021-07-21 | GSE157087 | GEO

AMPK activation reverts mouse epiblast stem cells to naïve state

Project description:Reversion from primed to naïve pluripotent status has been achieved by various signaling manipulation, but it is still unclear what signaling is the actual driving force to get over the hurdle from primed to naïve pluripotency. We previously reported that activation of AMP kinase (AMPK) contributed to maintenance of naïve pluripotency. Here, we further show that AMPK activators, AICAR, A769662 or metformin, can induce the reversion of primed mouse epiblast stem cells (mEpiSCs) to naïve pluripotent state. Primed mEpiSCs in our naïve cell culture condition with leukemia inhibitory factor (LIF) and 2 kinase inhibitors (2i) (2iL) never gave rise to naïve state cells. Addition of AICAR alone even in the absence of 2iL or either of AMPK inhibitors with LIF induced appearance of naïve-like cells from primed mEpiSCs. Through maintenance and passages of these cells in 2iL condition, clear naïve-like morphology colonies were purely obtained. They showed core naïve protein expression, and global naïve gene expression profiles. These cells contributed to chimeric mice including germline transmission. Inhibition of p38 signaling abolished the AMPK-elicited reversion and forced activation of p38 in primed mEpiSCs partially reproduced the naïve cell induction, suggesting that p38 is one of the critical downstream in AMPK activation. Single cell RNA-seq analysis under AICAR stimulation successfully demonstrated the reversion process with appearance of intermediate naïve-like population. AMPK pathway should be a novel critical driving force in reversion of primed to naïve pluripotency.

2021-07-21 | GSE175610 | GEO

Reduced Representation Bisulphite Sequencing of WT and AICDA KO iPCS clones

Project description:We report AICDA facilitates naïve pluripotency of mouse iPSCs by suppressing FGF/ERK signaling. In the absence of AICDA iPSCs fail to achive naïve pluripotent state and display chracteristics of EpiSCs and are primed for differentiation.

2019-04-03 | GSE129187 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data