Transcriptional profiling of LIF stimulation in mouse embryonic stem cells
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ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR318664.fastq.gz | Fastqsanger.gz | |||
| ERR318665.fastq.gz | Fastqsanger.gz | |||
| ERR318666.fastq.gz | Fastqsanger.gz | |||
| ERR318667.fastq.gz | Fastqsanger.gz | |||
| ERR318668.fastq.gz | Fastqsanger.gz |
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Project description:Stat3+/+ and -/- ES cells were cultured in defined conditions and exposed to leukemia inhibitory factor (LIF) in a 24h timecourse to identify Stat3-independent targets of the self-renewal response to LIF signaling.
2013-08-01 | E-MTAB-1796 | biostudies-arrayexpress
Project description:Description: The pluripotency of an embryonic stem cell makes it an attractive target for differentiation strategies aimed at producing tissues for therapeutic purposes. Yet, even though we know that ES cells have tremendous capacity for differentiation, we do not fully understand the molecular paths taken by these cells as they differentiate. In addition, it is unclear how important the removal of leukemia inhibitory factor is to ES cell differentiation. Moreover, it is unclear how the path of ES cell differentiation relates to the molecular decisions made by tissues undergoing normal development. The motivation behind this work is to increase our understanding of this relationship and its potential limitations. Dataset is a murine embryonic stem cell differentiation timecourse consisting of 14 timepoints spanning 17 days of differentiation. Samples were harvested at 24 hour intervals on days 0,1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 13, 15, and 17. There two replicates of each sample in this series. Additionally, there are 14 identically stated differentiation samples, where growth was conducted in ES cell media containing LIF. A common reference design was employed. Groups of assays that are related as part of a time series. Compound Based Treatment: Treatment or lack of treatment with LIF Elapsed Time: Samples were harvested at 24 hour intervals on days 0,1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 13, 15, and 17 Keywords: time_series_design
2010-09-09 | GSE9048 | GEO
Project description:Enhancers are distal regulators of gene expression that shape cell identity and regulate cell fate transitions. Mouse embryonic stem cells (mESCs) are a typical example of cells whose pluripotent identity is maintained by a complex enhancer landscape, that is drastically altered upon differentiation. Genome-wide chromatin accessibility and histone modification assays are commonly used as a proxy for enhancer location, strength and dynamics. Here, we applied STARR-seq, a genome-wide plasmid-based assay, to measure the enhancer potential of genomic loci in a plasmid context in “ground-state” (2i+LIF; 2iL-ESCs) and “metastable” (serum+LIF; SL-ESCs) embryonic stem cells.
2020-08-16 | GSE143544 | GEO
Project description:Description: The pluripotency of an embryonic stem cell makes it an attractive target for differentiation strategies aimed at producing tissues for therapeutic purposes. Yet, even though we know that ES cells have tremendous capacity for differentiation, we do not fully understand the molecular paths taken by these cells as they differentiate. In addition, it is unclear how important the removal of leukemia inhibitory factor is to ES cell differentiation. Moreover, it is unclear how the path of ES cell differentiation relates to the molecular decisions made by tissues undergoing normal development. The motivation behind this work is to increase our understanding of this relationship and its potential limitations. Dataset is a murine embryonic stem cell differentiation timecourse consisting of 14 timepoints spanning 17 days of differentiation. Samples were harvested at 24 hour intervals on days 0,1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 13, 15, and 17. There two replicates of each sample in this series. Additionally, there are 14 identically stated differentiation samples, where growth was conducted in ES cell media containing LIF. A common reference design was employed. Groups of assays that are related as part of a time series. Compound Based Treatment: Treatment or lack of treatment with LIF Elapsed Time: Samples were harvested at 24 hour intervals on days 0,1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 13, 15, and 17 Keywords: time_series_design Using regression correlation
2010-09-09 | E-GEOD-9048 | biostudies-arrayexpress
Project description:This experiment is part of the FunGenES project (FunGenES - Functional Genomics in Embryonic Stem Cells partially funded by the 6th Framework Programme of the European Union, http://www.fungenes.org). The experiment was conducted at the University Bordeaux 2 (CNRS UMR 5164). The purpose of the experiment was to identify the LIF-dependent genes and early differentiation markers in mouse ES cells. Leukemia Inhibitory Factor (LIF) is a member of the Interleukin-6 (IL-6) family of cytokines, which displays pleiotropic functions, depending on both cell maturity and cell type. LIF maintains ES cell pluripotency and is a critical cell survival factor in myocytes. Materials and methods: CGR8 cell line was used.6 cell conditions tested: + LIF, reinduced 25 min with serum + LIF reinduced 25 min with serum and LIF 500pM - LIF for 24h, reinduced 25 min with serum - LIF for 24h, reinduced 25 min with serum and LIF 500pM- LIF for 48h, reinduced 25 min with serum - LIF for 48h, reinduced 25 min with serum and LIF 500pM. Relationships between samples. 5 independent preparations of mRNA have been done on five different CGR8 passages. Culture conditions: Monolayer adherent cells. RNA isolation method: Qiagen column
2009-07-10 | E-TABM-667 | biostudies-arrayexpress
Project description:STARR-seq enhancer activity in mouse embryonic stem cells cultured in 2i+LIF or serum+LIF [STARR-seq]
| PRJNA600931 | ENA
Project description:This experiment records the transcriptional responses of mES cells (line OG2) to FGF/ERK stimulation in the presence of LIF, to LIF/STAT3 inhibition in the presence of an FGF/ERK inhibitor, and to combined FGF/ERK stimulation / LIF/STAT3 inhibition.
2010-02-21 | GSE17136 | GEO
Project description:The objective of this study was to identify genes regulated by canonical Wnt signaling in mouse embryonic stem cells (ESCs).Canonical Wnt signaling supports the pluripotency of mouse ESCs but also promotes differentiation of early mammalian cell lineages. To explain these paradoxical observations, we explored the gene regulatory networks at play. Canonical Wnt signaling is intertwined with the pluripotency network comprising Nanog, Oct4, and Sox2 in mouse ESCs. In defined media supporting the derivation and propagation of mouse ESCs, Tcf3 and ?-catenin interact with Oct4; Tcf3 binds to Sox motif within Oct-Sox composite motifs that are also bound by Oct4-Sox2 complexes. Further, canonical Wnt signaling up-regulates the activity of the Pou5f1 distal enhancer via the Sox motif in mouse ESCs. When viewed in the context of published studies on Tcf3 and ?-catenin mutants, our findings suggest that Tcf3 counters pluripotency by competition with Sox2 at these sites, and Tcf3 inhibition is blocked by ?-catenin entry into this complex. Wnt pathway stimulation also triggers ?-catenin association at regulatory elements with classic Lef/Tcf motifs associated with differentiation programs. The failure to activate these targets in the presence of a MEK/ERK inhibitor essential for mouse ESC culture suggests that MEK/ERK signaling and canonical Wnt signaling combine to promote mouse ESC differentiation. Triplicates of mouse embryonic stem cells cultured with GSK3 inhibitor CHIR99021 or with Wnt pathway inhibitor XAV939.
2013-03-01 | E-GEOD-43420 | biostudies-arrayexpress
Project description:The objective of this study was to identify genes regulated by canonical Wnt signaling in mouse embryonic stem cells (ESCs).Canonical Wnt signaling supports the pluripotency of mouse ESCs but also promotes differentiation of early mammalian cell lineages. To explain these paradoxical observations, we explored the gene regulatory networks at play. Canonical Wnt signaling is intertwined with the pluripotency network comprising Nanog, Oct4, and Sox2 in mouse ESCs. In defined media supporting the derivation and propagation of mouse ESCs, Tcf3 and β-catenin interact with Oct4; Tcf3 binds to Sox motif within Oct-Sox composite motifs that are also bound by Oct4-Sox2 complexes. Further, canonical Wnt signaling up-regulates the activity of the Pou5f1 distal enhancer via the Sox motif in mouse ESCs. When viewed in the context of published studies on Tcf3 and β-catenin mutants, our findings suggest that Tcf3 counters pluripotency by competition with Sox2 at these sites, and Tcf3 inhibition is blocked by β-catenin entry into this complex. Wnt pathway stimulation also triggers β-catenin association at regulatory elements with classic Lef/Tcf motifs associated with differentiation programs. The failure to activate these targets in the presence of a MEK/ERK inhibitor essential for mouse ESC culture suggests that MEK/ERK signaling and canonical Wnt signaling combine to promote mouse ESC differentiation.
2013-03-01 | GSE43420 | GEO
Project description:The TET family of FE(II) and 2-oxoglutarate-dependent enzymes (Tet1/2/3) promote DNA demethylation by converting 5-methylcytosine to 5-hydroxymethylcytosine (5hmC), which they further oxidize into 5-formylcytosine and 5-carboxylcytosine. Tet1 is robustly expressed in mouse embryonic stem cells (mESCs) and has been implicated in mESC maintenance. Here we demonstrate that, unlike genetic deletion, RNAi-mediated depletion of Tet1 in mESCs led to a significant reduction in 5hmC and loss of mESC identity. The differentiation phenotype due to Tet1 depletion positively correlated with the extent of 5hmC loss. Meta-analyses of genomic datasets suggested interaction between Tet1 and leukemia inhibitory factor (LIF) signaling. LIF signaling is known to promote self-renewal and pluripo-tency in mESCs partly by opposing MAPK/ERK mediated differentiation. Withdrawal of LIF leads to differentiation of mESCs. We discovered that Tet1 depletion impaired LIF-dependent Stat3-mediated gene activation by affecting Stat3's ability to bind to its target sites on chromatin. Nanog overexpression or inhibition of MAPK/ERK signaling, both known to maintain mESCs in the absence of LIF, rescued Tet1 depletion, further supporting the dependence of LIF/Stat3 signaling on Tet1. These data support the conclusion that analysis of mESCs in the hours/days immediately following efficient Tet1 depletion reveals Tet1’s normal physiological role in maintaining the pluripotent state that may be subject to homeostatic compensation in genetic models.
2012-01-06 | GSE34886 | GEO