Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

25 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq from wt oocytes

ABSTRACT: To determine gene expression in mouse ovulated oocytes 3 Replicates of litters of wild type ovulated oocytes

ORGANISM(S): Mus musculus

SUBMITTER: Todd Macfarlan

PROVIDER: E-GEOD-33922 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Embryonic stem cell potency fluctuates with endogenous retrovirus activity.

Macfarlan Todd S TS Gifford Wesley D WD Driscoll Shawn S Lettieri Karen K Rowe Helen M HM Bonanomi Dario D Firth Amy A Singer Oded O Trono Didier D Pfaff Samuel L SL

Nature 20120701 7405

Embryonic stem (ES) cells are derived from blastocyst-stage embryos and are thought to be functionally equivalent to the inner cell mass, which lacks the ability to produce all extraembryonic tissues. Here we identify a rare transient cell population within mouse ES and induced pluripotent stem (iPS) cell cultures that expresses high levels of transcripts found in two-cell (2C) embryos in which the blastomeres are totipotent. We genetically tagged these 2C-like ES cells and show that they lack t ...[more]

PMID: 22722858

Similar Datasets

2C::tomato ES cells, 2-cell embryos and wild type oocytes

Project description:This SuperSeries is composed of the following subset Series: GSE33763: Expression data from 2C::tomato+ vs 2C::tomato - ES cells GSE33920: mRNA-Seq of 2C::tomato+ vs. - ES cells GSE33921: RNA-Seq from two-cell (2C) stage embryos GSE33922: RNA-Seq from wt oocytes GSE36896: RNA-Seq from wt and G9A knockout ES cells Refer to individual Series

2012-06-17 | E-GEOD-33923 | biostudies-arrayexpress

RNA-Seq from two-cell (2C) stage embryos

Project description:To determine gene expression in 2 cell stage embryos 3 Replicates of litters of wild type 2 cell stage embryos

2012-06-18 | E-GEOD-33921 | biostudies-arrayexpress

mRNA-Seq of 2C::tomato+ vs. - ES cells

Project description:We identified/quantified genes and repeat elements enriched within 2C::tomato+ cells vs. 2C::tomato - cells 2C::tomato + and - cells were collected by FACS for RNA-Seq analysis

2012-06-18 | E-GEOD-33920 | biostudies-arrayexpress

A comparative epigenomics approach reveals REST as a mediator of Polycomb reprogramming during neuronal differentiation

Project description:Transcription factors (TFs) in concert with chromatin pathways stably reset transcriptional programs during differentiation. Yet we know little how local sites of chromatin reprogramming are specified and how the estimated 3000 TF encoded in mammalian genomes contribute to chromatin dynamics. To identify candidate TFs we developed an integrated computational approach (Epi-MARA) that models chromatin dynamics in terms of predicted transcription factor binding sites and show that it correctly predicts key TFs involved in epigenome reorganization. When applied to a time course of genome-wide H3 lysine 27 trimethylation (H3K27me3), a chromatin mark set by the Polycomb system, during neuronal differentiation of murine stem cells Epi-MARA predicted that the repressive transcription factor REST contributes to a gain of H3K27me3 at a subset of promoters during the transition from the stem to the progenitor state. To test this prediction we identified, genome-wide, the actual binding sites of REST and H3K27me3 during the differentiation in cells that are either wildtype or in which REST had been deleted. REST indeed localizes to a subset of sites that gain H3K27me3 in progenitors. Importantly, absence of REST in trans leads to a loss of H3K27me3 predominantly in the neuronal progenitor state and specifically at those regions where REST was bound. This function further requires REST binding sites in cis as their mutation leads to substantial loss of H3K27me3. Taken together we provide a novel approach to identify epigenome and TF crosstalk during cellular reprogramming and prove experimentally the prediction that REST acts as an important recruiter of Polycomb repression during early steps of neurogenesis. Dataset comprises of 15 ChIP-seq samples using chromatin from embryonic stem (ES) and neuronal progentor (NP) of wildtype and RESTko cells, which was immunoprecipitated, using antibodies against REST, H3K27me3, or Suz12

2012-09-04 | E-GEOD-27148 | biostudies-arrayexpress

A unique role of Cohesin-SA1 in gene regulation and development [ChIP-Seq]

Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Examination of genome wide distribution of cohesin subunits in wildtype and SA1-null cells

2012-03-15 | E-GEOD-32319 | biostudies-arrayexpress

Kinetic RNA polymerase II occupancy, associated histone marks, and mRNA accumulation reveal transcriptional and post-transcriptional mechanisms underlying circadian gene expression

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

2012-12-06 | E-GEOD-35790 | biostudies-arrayexpress

Genome-wide profiles of RNA polymerase II (Pol 2) DNA occupancy and the histone modifications H3K4me3 and H3K36me3 around the circadian cycle

Project description:To understand the transcriptional basis of circadian rhythms in mouse liver, we generated genome-wide profiles of RNA polymerase II (Pol 2) DNA occupancy and the histone modifications H3K4me3 and H3K36me3 around the circadian cycle. We found that Pol 2 occupancy at promoters and in gene bodies cycle in synchrony, suggesting that Pol 2 recruitment at promoters underlies circadian gene transcription. On average, Pol 2 occupancy precedes mRNA accumulation by about three hours. Promoters of transcribed genes have tri-methylated H3K4 residues even at their trough activity times, and the tri-methylation levels increase in phase with Pol 2 loading. In contrast, the tri-methylation of H3K36 residues lags transcription by three hours with amplitudes that are markedly shallower, indicating that this mark is less dynamic on the circadian time scale. The comparison of Pol 2 occupancy and mRNA accumulation revealed that both transcriptional and post-transcriptional regulatory mechanisms can account for diurnal mRNA profiles. Additional processed data and visualization tools are available at http://cyclix.vital-it.ch/ Contributed by members of CycliX consortium (http://cyclix.vital-it.ch/) 28 samples examinded, 7 Polr2b, 7 H3K4me3, 7 H3k36me3, 7 input samples.

2012-12-06 | E-GEOD-35788 | biostudies-arrayexpress

RNA-Seq from wt and G9A knockout ES cells

Project description:To measure gene expression difference between wt and g9A knockout ES cells G9A TT2 ES cells (Yokochi et al) were treated with Veh. Or 4OHT (to delete G9A)

2012-06-18 | E-GEOD-36896 | biostudies-arrayexpress

Dynamics of SREBP1 binding to DNA in mouse liver

Project description:To systematically understand how the circadian clock and the nutrient-driven rhythm integrate to regulate SREBP1 activity, we evaluated genome-wide the binding of SREBP1 to its targets along the day in wild-type (WT) C57BL/6mice. The recruitment of SREBP1 to the DNA showed a highly circadian behaviour, with a maximum during the fed status. However, the temporal expression of SREBP1 targets was not always synchronized with its binding. In particular, a different phase of expression was observed for SREBP1 target genes depending on their function, suggesting the involvement of other transcription factors in their regulation. The proper temporal expression pattern of these genes was dramatically changed in Bmal1KO mice upon time-restricted feeding, in spite of the rhythmic, although slightly delayed, binding of SREBP1. Our results show that besides the nutrient-driven regulation of SREBP1 nuclear translocation, a second layer of modulation of SREBP1 transcriptional activity exists and is strongly dependent from the circadian core clock. This system allows to fine tune the expression timing of SREBP1 target genes, thus helping to temporally separate the different physiological processes in which these genes are involved. 6 samples examined, 6 SREBP1 samples, as well as 6 Polr2b and 6 input samples from GEO series GSE35788 CycliX Consortium was a contributor to this submission.

2014-03-10 | E-GEOD-48375 | biostudies-arrayexpress

Suppression of the antiviral response by an influenza "histone mimic"

Project description:Viral infection is commonly associated with virus-driven hijacking of host proteins. We describe a novel mechanism by which influenza virus impacts host cells through the interaction of influenza NS1 protein with the infected cell epigenome. We show that the NS1 protein of influenza A H3N2 target the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. In the following data sets, we show that NS1 colocalizes with hPAF1 on the chromatin of infected cells and that siRNA-mediated reduction of hPAF1 expression results in reduced recruitment of NS1 to the chromatin. Examination of different histone modifications in infected cells and RNA-Seq and GRO-Seq transcript measurements.

2013-07-01 | E-GEOD-35774 | 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