Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Felix Krueger

PROVIDER: E-GEOD-62150 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast.

Cambuli Francesco F Murray Alexander A Dean Wendy W Dudzinska Dominika D Krueger Felix F Andrews Simon S Senner Claire E CE Cook Simon J SJ Hemberger Myriam M

Nature communications 20141126

Embryonic (ES) and trophoblast (TS) stem cells reflect the first, irrevocable cell fate decision in development that is reinforced by distinct epigenetic lineage barriers. Nonetheless, ES cells can seemingly acquire TS-like characteristics upon manipulation of lineage-determining transcription factors or activation of the extracellular signal-regulated kinase 1/2 (Erk1/2) pathway. Here we have interrogated the progression of reprogramming in ES cell models with regulatable Oct4 and Cdx2 transgen ...[more]

PMID: 25423963

Similar Datasets

Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast [MeDIP-Seq]

Project description:Reprogramming of ES cells towards the trophoblast lineage, and specifally into self-renewing TS cells, can seemingly be achieved by manipulation of transcription factors such as Cdx2 and Oct4, or modulation of signalling cascades, notably Ras signalling. Here we analyze the arising cells from such treatment in detail for the efficiency and completeness of the reprogramming process. We find that the reprogrammed cells retain an epigenetic and transcriptional memory of their ES cell origin and are not equal to bona fide trophectoderm-derived TS cells. DNA methylation analysis in conventional ES and TS cells and various ES-to-TS reprogramming models

2014-11-24 | E-GEOD-62138 | biostudies-arrayexpress

Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast [RNA-Seq]

Project description:Reprogramming of ES cells towards the trophoblast lineage, and specifally into self-renewing TS cells, can seemingly be achieved by manipulation of transcription factors such as Cdx2 and Oct4, or modulation of signalling cascades, notably Ras signalling. Here we analyze the arising cells from such treatment in detail for the efficiency and completeness of the reprogramming process. We find that the reprogrammed cells retain an epigenetic and transcriptional memory of their ES cell origin and are not equal to bona fide trophectoderm-derived TS cells. RNA-seq expression analysis in conventional ES and TS cells and various ES-to-TS reprogramming models

2014-11-24 | E-GEOD-62149 | biostudies-arrayexpress

Conditional knockout of Sox2 in embryonic and trophoblast stem cells.

Project description:To compare the transcriptional networks governed by Sox2 in embryonic stem (ES) cells and trophoblast stem (TS) cells, we performed whole-genome expression analysis after tetracycline (Tet)-induced knockout of Sox2 in each cell type. A Tet-inducible Sox2 knockout ES cell line 2TS22C or its derivative TSC line 22CEROH2-TSC1 were treated with Tet for 4 days. A total of 12 samples from ES or TS cells cultured with or without Tet were analyzed in three biological replicates.

2013-10-17 | E-GEOD-28451 | biostudies-arrayexpress

Sox2-regulatory networks in embryonic and trophoblast stem cells.

Project description:Sox2 is a pleiotropic transcription factor that regulates self-renewal and differentiation capacity in different types of stem cells, raising the possibility that it regulates similar transcriptional programs controlling common stemness. Embryonic stem (ES) cells and trophoblast stem (TS) cells are two developmentally related types of stem cells, which originate from distinct lineages of peri-implantation embryos. We have found that Sox2 is a critical regulator of self-renewal in both of two stem cells. Genome-wide analysis of Sox2 target genes using Affymetrix Exon Arrays and chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) unraveled that it regulates distinct transcriptional networks in ES and TS cells. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-10-17 | E-GEOD-28455 | biostudies-arrayexpress

Lsd1 coordinates trophoblast development by retaining stem cells in their niche and directing cell fate

Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation. Mouse trophoblast stem cells (TSCs) were isoloated from a single conditional Lsd1-deficient mouse (Lsd1tm1SchM-CM-<le). Deletion of Lsd1 was induced eight days before the collection of RNA by addition of 0.2 M-BM-5M 4OH-tamoxife. Cells were isolated at successive stages of differentiation for total RNA extraction and hybridization on Affymetrix microarrays. To that end, we harvested cells at three time-points: before induction of differentiation (d0), two days after induction of differentiation (d2), and four days after induction of differentiation (d4). Three replicates (1, 2, 3) for control (-) and Lsd1-deficeint (+) cells were included for each differentiation stage.

2014-01-17 | E-GEOD-38277 | biostudies-arrayexpress

Integrated detection of both 5-mC and 5-hmC by high-throughput tag sequencing technology highlights methylation reprogramming of bivalent genes during cellular differentiation [MeDIP_hMeDIP]

Project description:5-methylcytosine (5-mC) can be oxidized to 5-hydroxymethylcytosine (5-hmC). Genome-wide profiling of 5-hmC thus far indicated 5-hmC may not only be an intermediate form of DNA demethylation but could also constitute an epigenetic mark per se. We describe a cost-effective and selective method to detect both the hydroxymethylation and methylation status of cytosines in more than 1.8 million MspI sites in the human genome. This method involves the selective glucosylation of 5-hmC residues, short-sequence tag generation and high-throughput sequencing. We tested this method by screening H9 human embryonic stem cells and their differentiated embroid body cells, and found that differential hydroxymethylation preferentially occur in bivalent genes during cellular differentiation. Especially, our results support hydroxymethylation can regulate key transcription regulators with bivalent marks through demethylation and affect cellular decision on choosing active or inactive state of these genes upon cellular differentiation. We developed a cost-effective and selective method to detect both the hydroxymethylation and methylation status of cytosines in more than 1.8 million MspI sites in the human genome. In order to validate the results generated by this method, we applied MeDIP-seq and hMeDIP-seq to screen H9 human embryonic stem cells in comparison with the newly developed method.

2012-12-20 | E-GEOD-41070 | biostudies-arrayexpress

H2A.B facilitates transcription at methylated CpG Loci

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-12-24 | E-GEOD-49294 | biostudies-arrayexpress

H2A.B and MeDIP sequence result

Project description:H2A.B is a unique histone H2A variant that shares only 40 ~ 50 % sequence identity with canonical H2A. It has only been identified in mammals and has quickly evolved with remarkable sequence diversity among different species. H2A.B is ubiquitously expressed in most cells and tissues. It is mainly deposited in gene body region. The localization of H2A.B is associated with methylated CpG islands in mouse ES cells. H2A.B facilitates transcription elongation to go through methylated CpG islands in the gene bodies. One typical example is that H2A.B regulates transcription elongation at imprinted loci. We found H2A.B enriched in some methylated loci. Using ChIP-seq and MeDIP-seq, we test the correlation of H2A.B and DNA methylation.

2013-12-24 | E-GEOD-48892 | biostudies-arrayexpress

ChIP-Seq of chromatin marks at distal enhancers in Mouse Embryonic Stem Cells and adult tissues.

Project description:Enhancers are enriched by histone H3 lysine 4 mono methylation (H3K4me1). To gain insight into the relation between enhancers and developmental state, chromatin immunoprecipitation coupled with massive parallel sequencing (ChIP-seq) was performed in several cell types to determine the genome-wide binding targets of H3K4me1 and several other possible enhancer associated modifications. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A chromatin IP against histone H3 or whole cell extract was sequenced and used as the background to determine enrichment. ChIP was performed mainly using antibodies against the chromatin marks H3K4me1 and H3K27ac.

2010-10-31 | E-GEOD-24164 | biostudies-arrayexpress

DNA Methylation Profiles Define Stem Cell Identity and Reveal a Tight Embryonic-Extraembryonic Lineage Boundary

Project description:Embryonic (ES) and epiblast (EpiSC) stem cells are pluripotent but committed to an embryonic lineage fate. Conversely, trophoblast (TS) a nd extraembryonic endoderm (XEN) stem cells contribute predominantly to tissues of the placenta and yolk sac, respectively. Here we show that each of these four stem cell types is defined by a unique DNA methylation profile. Despite their distinct developmental origin, TS and XEN cells share key epigenomic hallmarks, chiefly characterized by robust DNA methylation of embryo-specific developmental regulators, as well as a subordinate role of 5-hydroxymethylation. We also observe a substantial methylation reinforcement of pre-existing epigenetic repressive marks that specifically occurs in extraembryonic stem cells compared to in vivo tissue, presumably due to continued high Dnmt3b expression levels. These differences establish a major epigenetic barrier between the embryonic and extraembryonic stem cell types. In addition, epigenetic lineage boundaries also separate the two extraembryonic stem cell types by mutual repression of key lineage-specific transcription factors. Thus, global DNA methylation patterns are a defining feature of each stem cell type that underpin lineage commitment and differentiative potency of early embryo-derived stem cells. Our detailed methylation profiles identify a cohort of developmentally regulated sequence elements, such as orphan CpG islands, that will be most valuable to uncover novel transcriptional regulators and pivotal M-^QM-^QgatekeeperM-^RM-^R genes in pluripotency and lineage differentiation.

2013-07-03 | E-MTAB-1754 | biostudies-arrayexpress

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