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Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning

ABSTRACT: Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning

PROVIDER: PRJNA288980 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2087750_1.fastq.gz	Fastqsanger.gz
	SRR2087750_2.fastq.gz	Fastqsanger.gz
	SRR2087741_1.fastq.gz	Fastqsanger.gz
	SRR2087741_2.fastq.gz	Fastqsanger.gz
	SRR2087751_1.fastq.gz	Fastqsanger.gz

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Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning [ChIP-Seq]

Project description:Following implantation, mouse epiblast cells transit from a naïve to a primed state in which they are competent for both somatic and primordial germ cell (PGC) specification. Using mouse embryonic stem cells (mESC) as an in vitro model to study the transcriptional regulatory principles orchestrating peri-implantation development, here we show that the transcription factor Foxd3 is necessary for the exit from naïve pluripotency and the progression to a primed pluripotent state. During this transition, Foxd3 acts as a repressor that dismantles a significant fraction of the naïve pluripotency expression program through the decommissioning of active enhancers associated with key naïve pluripotency and early germline genes. Subsequently, Foxd3 needs to be silenced in primed pluripotent cells to allow the reactivation of relevant genes required for proper PGC specification. Our findings uncover a wave of activation-deactivation of Foxd3 as a crucial step for the exit from naïve pluripotency and subsequent PGC specification. Genome-wide binding profiles for Foxd3 were investigated in mouse embryonic stem cells (mESC). A mESC line (FH-Foxd3 mESC line) expressing exogenous Foxd3 tagged with Flag and HA epitope (FH-Foxd3) at nearly endogenous levels was generated. ChIPs were performed against FH-Foxd3 using anti-HA or anti-Flag antibodies.

2015-09-14 | E-GEOD-70545 | biostudies-arrayexpress

Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning [RNA-Seq]

Project description:Following implantation, mouse epiblast cells transit from a naïve to a primed state in which they are competent for both somatic and primordial germ cell (PGC) specification. Using mouse embryonic stem cells (mESC) as an in vitro model to study the transcriptional regulatory principles orchestrating peri-implantation development, here we show that the transcription factor Foxd3 is necessary for the exit from naïve pluripotency and the progression to a primed pluripotent state. During this transition, Foxd3 acts as a repressor that dismantles a significant fraction of the naïve pluripotency expression program through the decommissioning of active enhancers associated with key naïve pluripotency and early germline genes. Subsequently, Foxd3 needs to be silenced in primed pluripotent cells to allow the reactivation of relevant genes required for proper PGC specification. Our findings uncover a wave of activation-deactivation of Foxd3 as a crucial step for the exit from naïve pluripotency and subsequent PGC specification. mRNA profiles were generated by RNA-seq in duplicates for each of the following mESC lines: Foxd3fl/fl;Cre-ER mESC maintained in "Serum+LIF" (SL) treated with TM for three days (SL Foxd3-/-); untreated Foxd3fl/fl;Cre-ER SL mESC (SL Foxd3fl/fl); tetON Foxd3 SL mESC treated with Dox for three days; WT SL mESC treated with Dox for three days; Foxd3fl/fl;Cre-ER mESC maintained in "2i+LIF" (2i) treated with TM for three days (2i Foxd3-/-); untreated Foxd3fl/fl;Cre-ER 2i mESC (2i Foxd3fl/fl).

2015-09-14 | E-GEOD-70546 | biostudies-arrayexpress

Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning [RNA-Seq]

2015-09-14 | GSE70546 | GEO

Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning [ChIP-Seq]

2015-09-14 | GSE70545 | GEO

Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning

Project description:Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning

| PRJNA288980 | ENA

Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning

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

2015-09-14 | E-GEOD-70547 | biostudies-arrayexpress

Foxd3 promotes the exit from naïve pluripotency and prevents germline specification through enhancer decommissioning

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

2015-09-14 | GSE70547 | GEO

Foxd3 Promotes Exit from Naive Pluripotency through Enhancer Decommissioning and Inhibits Germline Specification.

Project description:Following implantation, mouse epiblast cells transit from a naive to a primed state in which they are competent for both somatic and primordial germ cell (PGC) specification. Using mouse embryonic stem cells as an in vitro model to study the transcriptional regulatory principles orchestrating peri-implantation development, here we show that the transcription factor Foxd3 is necessary for exit from naive pluripotency and progression to a primed pluripotent state. During this transition, Foxd3 acts as a repressor that dismantles a significant fraction of the naive pluripotency expression program through decommissioning of active enhancers associated with key naive pluripotency and early germline genes. Subsequently, Foxd3 needs to be silenced in primed pluripotent cells to allow re-activation of relevant genes required for proper PGC specification. Our findings therefore uncover a cycle of activation and deactivation of Foxd3 required for exit from naive pluripotency and subsequent PGC specification.

| S-EPMC5048917 | biostudies-literature

Mi-2 and E93 coordinate robust cell cycle exit with terminal differentiation through enhancer decommissioning [RNA-seq]

Project description:Many postmitotic tissues coordinate robust cell cycle exit with the progression of terminal differentiation. While the signals involved in initiating cell cycle exit during terminal differentiation for some tissues have been described, less is known about the mechanisms that maintain a stable, non-cycling state. We previously found that chromatin accessibility changes at a subset of rate-limiting cell cycle genes occurs during maintenance of cell cycle exit, suggesting chromatin remodelers may play a key role in maintaining a robust postmitotic state during terminal differentiation. Here we show that the chromatin remodeler Mi-2 is required to ensure a stable, postmitotic state in Drosophila eyes and wings. Mi-2 alters chromatin accessibility and gene expression during cell cycle exit and terminal differentiation. Mi-2 and a transcription factor involved in tissue maturation, E93, close chromatin accessibility at an overlapping subset of potential enhancers that include the rate-limiting mitotic regulator string (cdc25c) and genes involved in the progression of terminal differentiation. E93 is also required for a stable, postmitotic state and we verified in vivo that Mi-2 and E93 cooperate to decommission an enhancer for the essential mitotic regulator string, to coordinate the transition to a postmitotic state with terminal differentiation. Enhancer decommissioning at the string locus provides a molecular explanation for the long-term, nearly irreversible postmitotic state observed in many tissues as terminal differentiation progresses.

2024-06-26 | GSE259303 | GEO

Mi-2 and E93 coordinate robust cell cycle exit with terminal differentiation through enhancer decommissioning [ATAC-seq]

2024-06-26 | GSE259302 | GEO