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Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [RNA-Seq]

ABSTRACT: Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [RNA-Seq]

PROVIDER: PRJNA1063676 | ENA |

REPOSITORIES: ENA

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Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [RNA-Seq]

Project description:Epigenetic control of cell type is a critical determinant in cell type stability and permissive differentiation. However, the epigenetic control mechanisms are not well understood. Here, we explore the epigenetic control of the conversion of primed mouse EpiSCs to naïve mouse ESCs as a mimic for early stages of embryonic development. Whilst the conversion of naïve to primed state is relatively permissive and mimics a normal developmental program, the reverse process, primed to naïve is inefficient in the absence of transgenes, which suggests the presence of potent epigenetic barriers that resist this artificial dedifferentiation. Here, we identify the histone acetylation reader BRD8 as a one-way barrier that blocks the conversion of primed to naïve cells. BRD8 works by maintaining histone acetylation on promoters and transcribed gene bodies and it’s absence promotes the formation of heterochromatin.

2024-12-08 | GSE253031 | GEO

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ChIP-Seq]

2024-12-08 | GSE253030 | GEO

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ATAC-Seq]

2024-12-08 | GSE253029 | GEO

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs

Project description:Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs

| PRJNA1063672 | ENA

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ChIP-Seq]

Project description:Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ChIP-Seq]

| PRJNA1063677 | ENA

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ATAC-Seq]

Project description:Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs [ATAC-Seq]

| PRJNA1063678 | ENA

Epigenetic modulation through BRD8 impairs conversion of primed EpiSCs to naïve ESCs

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

2024-12-07 | GSE253033 | GEO

OCT4 IP-MS in Naive and Primed Human ESCs

Project description:Understanding the molecular underpinnings of pluripotency is a prerequisite for optimal maintenance and application of embryonic stem cells (ESCs). While the protein-protein interactions of core pluripotency factors have been identified in mouse ESCs, their interactome in human ESCs (hESCs) has not to date been explored. Here we mapped the OCT4 interactomes in naïve and primed hESCs, revealing extensive connections to mammalian ATP-dependent nucleosome remodeling complexes.

2021-09-12 | PXD026556 | Pride

c-JUN is a pioneer factor safeguarding the primed state of pluripotency (RNA-Seq)

Project description:Mouse ESCs and EpiSCs represent naive and primed states of plurioptency corresponding to two consecutive stages of embryo development. Here we map their chromatin accessibility landscapes and show that naive specific open chromatin are enriched with motifs for Oct/Sox/Klf/TCF and primed one with AP1 motifs. The AP1 founding member c-Jun is expressed in EpiSCs and occupies both open and closed chromatin. Yet, c-Jun deficiency has no impact on the self renewal nor the transcription program of EpiSCs. However, in a Klf4-driven reprogramming system, we show that c-Jun-/- EpiSCs undergo primed to naive transition more efficiently than wild type cells and Klf4 evicts c-JUN from wild type chromatin. These results suggest that c-Jun is a pioneer factor not to regulate transcription but to prevent backward reprogramming during naive-primed transition, thus providing a molecular basis for the forward principle in development.

2020-12-31 | GSE127925 | GEO

c-JUN is a pioneer factor safeguarding the primed state of pluripotency (ATAC-Seq)

Project description:Mouse ESCs and EpiSCs represent naive and primed states of plurioptency corresponding to two consecutive stages of embryo development. Here we map their chromatin accessibility landscapes and show that naive specific open chromatin are enriched with motifs for Oct/Sox/Klf/TCF and primed one with AP1 motifs. The AP1 founding member c-Jun is expressed in EpiSCs and occupies both open and closed chromatin. Yet, c-Jun deficiency has no impact on the self renewal nor the transcription program of EpiSCs. However, in a Klf4-driven reprogramming system, we show that c- Jun-/- EpiSCs undergo primed to naive transition more efficiently than wild type cells and Klf4 evicts c-JUN from wild type chromatin. These results suggest that c-Jun is a pioneer factor not to regulate transcription but to prevent backward reprogramming during naive-primed transition, thus providing a molecular basis for the forward principle in development.

2020-12-31 | GSE127920 | GEO

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