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Epigenomic comparison of distinct pluripotent stem cell states reveals a new class of enhancers with roles throughout mammalian development (ChIP-seq)

ABSTRACT: Naïve mouse embryonic stem cells (mESCs) and primed epiblast stem cells (mEpiSCs) represent successive snapshots of pluripotency during embryogenesis. Using transcriptomic and epigenomic mapping, we show that a small fraction of transcripts are differentially expressed between mESCs and mEpiSCs and these genes show expected changes in chromatin at their promoters and enhancers. Unexpectedly, the cis-regulatory circuitry of genes that are expressed at identical levels between these cell states also differs dramatically. In mESCs, these genes are associated with dominant proximal enhancers and dormant distal enhancers, which we term seed enhancers. In mEpiSCs, the naïve-dominant enhancers are lost, and the seed enhancers take up primary transcriptional control. Seed enhancers have increased sequence conservation and show preferential usage in downstream somatic tissues, often expanding into super enhancers. We propose that seed enhancers ensure proper enhancer utilization and transcriptional fidelity as mammalian cells transition from naïve pluripotency to a somatic regulatory program.

ORGANISM(S): Mus musculus

PROVIDER: GSE57407 | GEO | 2014/06/04

SECONDARY ACCESSION(S): PRJNA246398

REPOSITORIES: GEO

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Epigenomic comparison of distinct pluripotent stem cell states reveals a new class of enhancers with roles throughout mammalian development (RNA-seq)

Project description:Naïve mouse embryonic stem cells (mESCs) and primed epiblast stem cells (mEpiSCs) represent successive snapshots of pluripotency during embryogenesis. Using transcriptomic and epigenomic mapping, we show that a small fraction of transcripts are differentially expressed between mESCs and mEpiSCs and these genes show expected changes in chromatin at their promoters and enhancers. Unexpectedly, the cis-regulatory circuitry of genes that are expressed at identical levels between these cell states also differs dramatically. In mESCs, these genes are associated with dominant proximal enhancers and dormant distal enhancers, which we term seed enhancers. In mEpiSCs, the naïve-dominant enhancers are lost, and the seed enhancers take up primary transcriptional control. Seed enhancers have increased sequence conservation and show preferential usage in downstream somatic tissues, often expanding into super enhancers. We propose that seed enhancers ensure proper enhancer utilization and transcriptional fidelity as mammalian cells transition from naïve pluripotency to a somatic regulatory program.

2014-06-04 | GSE57403 | GEO

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Epigenomic comparison of distinct pluripotent stem cell states reveals a new class of enhancers with roles throughout mammalian development (DNase-seq)

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Project description:Reversion from primed to naïve pluripotent status has been achieved by various signaling manipulation, but it is still unclear what signaling is the actual driving force to get over the hurdle from primed to naïve pluripotency. We previously reported that activation of AMP kinase (AMPK) contributed to maintenance of naïve pluripotency. Here, we further show that AMPK activators, AICAR, A769662 or metformin, can induce the reversion of primed mouse epiblast stem cells (mEpiSCs) to naïve pluripotent state. Primed mEpiSCs in our naïve cell culture condition with leukemia inhibitory factor (LIF) and 2 kinase inhibitors (2i) (2iL) never gave rise to naïve state cells. Addition of AICAR alone even in the absence of 2iL or either of AMPK inhibitors with LIF induced appearance of naïve-like cells from primed mEpiSCs. Through maintenance and passages of these cells in 2iL condition, clear naïve-like morphology colonies were purely obtained. They showed core naïve protein expression, and global naïve gene expression profiles. These cells contributed to chimeric mice including germline transmission. Inhibition of p38 signaling abolished the AMPK-elicited reversion and forced activation of p38 in primed mEpiSCs partially reproduced the naïve cell induction, suggesting that p38 is one of the critical downstream in AMPK activation. Single cell RNA-seq analysis under AICAR stimulation successfully demonstrated the reversion process with appearance of intermediate naïve-like population. AMPK pathway should be a novel critical driving force in reversion of primed to naïve pluripotency.

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