Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA207817 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR891748.fastq.gz | Fastqsanger.gz | |||
| SRR891749.fastq.gz | Fastqsanger.gz | |||
| SRR891750.fastq.gz | Fastqsanger.gz | |||
| SRR891751.fastq.gz | Fastqsanger.gz | |||
| SRR891752.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
Similar Datasets
Project description:RNA sequencing of Epiblast stem cells, nodal inhibited epiblast stem cells and embryonic samples
| PRJNA358283 | ENA
Project description:Human embryonic stem cells (hESCs) typically exhibit "primed" pluripotency, analogous to stem cells derived from the mouse post-implantation epiblast. This has led to a search for growth conditions that support self-renewal of hESCs akin to hypomethylated naïve epiblast cells in human pre-implantation embryos. We have discovered that reverting primed hESCs to a hypomethylated naïve state or deriving a new hESC line under naïve conditions results in the establishment of Stage Specific Embryonic Antigen 4 (SSEA4) negative hESC lines with a transcriptional program resembling the human pre-implantation epiblast. In contrast, we discovered that the methylome of naïve hESCs in vitro is distinct from the human epiblast in vivo with loss of DNA methylation at primary imprints and a lost "memory" of the methylation state of the human oocyte. This failure to recover the naïve epiblast methylation landscape appears to be a consistent feature of self-renewing hypomethylated naïve hESCs in vitro.
2016-02-04 | GSE76970 | GEO
Project description:Conversion of Epiblast Stem Cells to Embryonic Stem Cells by Small Molecules
| PRJNA118609 | ENA
Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis
2018-08-02 | MSV000082680 | GNPS
Project description:The TET dioxygenases erase mediate DNA dedemethylation in pre-implantation embryos and in primordial germ cells, yet limited studies address their contribution to the global gain of DNA methylation following implantation. Here, we show that Tet1 is expressed and non-redundantly contributes to 5-hydroxymethylctyosine (5hmC) non-redundantly in the pre-gastrulation mouse epiblast. Ablation of Tet1 in primed epiblast cells results in widespread loss of 5hmC associated with gain of 5-methylcytosine at CpG islands and promoters. Moreover, Tet1 is expressed, albeit at lower levels, in the extra-embryonic ectoderm. Tet1-deficiency in the pre-streak mouse embryos causes dysregulation of early lineage regulators in the epiblast and increased expression of metabolic genes in the extra-embryonic ectoderm. Our studies reveal a distinct role of Tet1 in regulating the methylome landscape of the post-implantation mammalian epiblast and a hitherto unknown gene repressive effect in the extra-embryonic lineage, providing insights into the early developmental origins of epigenetic-based basis of imprinting and developmental disorders.
2017-05-15 | GSE71744 | GEO
Project description:During mammalian pre-implantation development, the cells of the blastocyst’s inner cell mass differentiate into the epiblast and primitive endoderm lineages, which give rise to the fetus and extra-embryonic tissues, respectively. Extra-embryonic endoderm differentiation can be modeled in vitro by induced expression of GATA transcription factors in mouse embryonic stem cells. Here we use this GATA-inducible system to quantitatively monitor the dynamics of global proteomic changes during the early stages of this differentiation event and also investigate the fully differentiated phenotype, as represented by embryo-derived extra-embryonic endoderm (XEN) cells. Using mass spectrometry-based quantitative proteomic profiling with multivariate data analysis tools, we reproducibly quantified 2,336 proteins across three biological replicates and have identified clusters of proteins characterized by distinct, dynamic temporal abundance profiles. We first used this approach to highlight novel marker candidates of the pluripotent state and extra-embryonic endoderm differentiation. Through functional annotation enrichment analysis, we have shown that the downregulation of chromatin-modifying enzymes, the re-organization of membrane trafficking machinery and the breakdown of cell-cell adhesion are successive steps of the extra-embryonic differentiation process. Thus, applying a range of sophisticated clustering approaches to a time-resolved proteomic dataset has allowed the elucidation of complex biological processes which characterize stem cell differentiation and could establish a general paradigm for the investigation of these processes.
2015-06-13 | PXD001901 | Pride
Project description:Mapping N6-methyladenosine methylome in mouse embryonic stem cells
| PRJNA188519 | ENA
Project description:Primitive ectoderm cells (PE) in blastocysts represent the foundation of the pluripotent state, which is lost progressively during development. For example, development of epiblast cells from PE in postimplantation embryos is accompanied by transcriptional and epigenetic changes, including DNA methylation and X inactivation (Refs); these changes alter the nature of epiblast cells fundamentally, affecting their responsiveness to signaling molecules, and constitute a robust boundary that prevents their reversion to a PE-like state. Notably, epiblast cells unlike PE, are refractory to leukaemia inhibitory factor (LIF)/STAT3 signalling in vitro; instead, they respond to FGF/Activin to form self-renewing epiblast stem cells (EpiSCs) that are like human ES cells, which differ significantly from mouse embryonic stem cells (ES) derived from PE. However, here we show that under appropriate conditions, epiblast cells from postimplantation embryos can respond to LIF/STAT3/fetal calf serum (FCS), and undergo reprogramming to form embryonic stem cell -like cells (repiES: reprogrammed epiblast ES-like cells). Reprogramming of epiblast cells occurs progressively. First, they form colonies that retain key properties of epiblast cells (cEpi: cultured epiblast), which subsequently show erasure of epigenetic modifications, including DNA demethylation and X-reactivation to generate repiES. Analysis also revealed that repiES progressively acquire a transcriptome profile of ES cells that is distinct from cEpi and EpiSCs. In chimeras, repiES contributed to all the tissues, including germ cells. Thus, we show for the first time that reversion of epiblast cells to repiES phenotype entails progressive loss of phenotypic and epigenetic memory of epiblast cells. Our study provides insights into underlying mechanisms, and a tractable model for how signaling molecules induce epigenetic reprogramming of cells leading to an elemental pluripotent state.
2009-10-29 | GSE15487 | GEO
Project description:Comparison of the binding patterns of the Rest complex between embryonic stem cells and epiblast stem cells. (mE14)
| PRJDB1964 | ENA