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A Myc-driven self-reinforcing regulatory network maintains mouse embryonic stem cell identity

ABSTRACT: A Myc-driven self-reinforcing regulatory network maintains mouse embryonic stem cell identity

PROVIDER: PRJNA319265 | ENA |

REPOSITORIES: ENA

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A Myc-driven self-reinforcing regulatory network maintains mouse embryonic stem cell identity (BeadChip)

Project description:We address the molecular mechanisms through which Myc supports mESC identity, by performing gene expression profile analyses of Myc- and LIF-maintained ESCs, together with Epiblast Stem Cell (EpiSC), as a control for a primed state of stemness. We then investigated whether the Myc-driven self-reinforcing circuit, installed in Myc-dependent ESCs, could support the maintenance of ES cell identity in absence of the originating stimulus, namely the MycER activation achieved by OHT stimulation. To this end, we derived ESCs from Myc-dependent cells, following MycER inactivation upon withdrawal of OHT and profile their gene expression.

2016-03-31 | GSE58656 | GEO

A Myc-driven self-reinforcing regulatory network maintains mouse embryonic stem cell identity.

Project description: Not available

| S-EPMC4912626 | biostudies-literature

A Myc-driven self-reinforcing regulatory network maintains mouse embryonic stem cell identity

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-04-22 | GSE80558 | GEO

A Myc-driven self-reinforcing regulatory network maintains mouse embryonic stem cell identity (ChIP-Seq)

Project description:Genome-wide mapping of H3K4me3, H3K27me3, SUZ12 in mESCs

2016-04-22 | GSE80557 | GEO

MafB maintains β-cell identity under MafA-deficient condition

Project description:MafB maintains β-cell identity under MafA-deficient condition

| PRJNA824305 | ENA

Mus musculus

Project description:A Myc-driven self-reinforcing regulatory network maintains mouse embryonic stem cell identity (ChIP-Seq)

| PRJNA319266 | ENA

RNA methylation maintains hematopoietic stem cell identity and symmetric commitment

Project description:RNA methylation maintains hematopoietic stem cell identity and symmetric commitment

| PRJNA547716 | ENA

Id1 maintains embryonic stem cell self-renewal by upregulation of Nanog and repression of Brachyury expression

Project description:Understanding the mechanism by which embryonic stem (ES) cells self-renew is critical for the realization of their therapeutic potential. Previously it had been shown that in combination with LIF, Id proteins were sufficient to maintain mouse ES cells in a self-renewing state. Here we investigate the requirement for Id1 in maintaing ES cell self-renewal and blocking differentiation. We find that Id1-/- ES cells have a propensity to differentiate and a decreased capacity to self-renew. Chronic or acute loss of Id1 leads to a down-regulation of Nanog, a critical regulator of self-renewal. In addition, in the absence of Id1, ES cells express elevated levels of Brachyury, a marker of mesendoderm differentiation. We find that loss of both Nanog and Id1 is required for the up-regulation of Brachyury, and Id1 maintains Nanog expression by blocking the expression of Zeb1, a repressor of Nanog transcription. These results identify Id1 as an important factor in the maintenance of ES cell self-renewal and suggest a plausible mechanism for its control of lineage commitment. Wild type and Id1-/- ES cells were grown on gelatin under normal self-renewing conditions (in the presence of serum and LIF).

2011-11-01 | E-GEOD-19144 | biostudies-arrayexpress

DNMT1 Maintains Progenitor Function in Self-Renewing Somatic Tissue

Project description:Progenitor cells maintain self-renewing tissues throughout life by sustaining their capacity for proliferation while suppressing cell cycle exit and terminal differentiation. DNA methylation provides a potential epigenetic mechanism for the cellular memory needed to preserve the somatic progenitor state through repeated cell divisions. DNA methyltransferase 1 (DNMT1) maintains DNA methylation patterns after cellular replication. Although dispensable for embryonic stem cell maintenance, a clear role for DNMT1 in maintaining the progenitor state in constantly replenished somatic tissues, such as mammalian epidermis, is uncharacterized. Here we show that DNMT1 is essential for supporting epidermal progenitor cell function. DNMT1 protein was found enriched in undifferentiated cells, where it was required to retain proliferative stamina and suppress differentiation. In tissue, DNMT1 depletion led to exit from the progenitor cell compartment, premature differentiation and eventual tissue loss. These effects correlated with DNA methylation as genome-wide analysis revealed that a significant portion of epidermal differentiation gene promoters were methylated in self-renewing conditions but were subsequently demethylated during differentiation. Gene expression analysis: To establish a differentiation signature for primary human keratinocytes, total RNA was isolated in biologic duplicate from cells cultured in growth conditions and high calcium differentiation conditions and hybridized to Affymetrix HG-U133 2.0 Plus arrays. This gene signature was also compared to DNMT1 deficient cells cultured in growth conditions. Methylated DNA profiling: To globally characterize DNA methylation in primary human keratinocytes, genomic DNA was immunoprecipitated using a 5-methylcytidine antibody, amplified, and hybridized to NimbleGen HG18 promoter tiling arrays. Profiling was done using DNA isolated in growth conditions as well as differentiation conditions.

2010-06-23 | E-GEOD-18590 | biostudies-arrayexpress

GIMAP5 maintains liver sinusoidal endothelial cell identity and prevents portal hypertension

Project description:GIMAP5 maintains liver sinusoidal endothelial cell identity and prevents portal hypertension

| PRJNA667260 | ENA