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Identification of regulators of exit from naïve pluripotent state by enhancer trap integration site mapping

ABSTRACT: Identification of regulators of exit from naïve pluripotent state by enhancer trap integration site mapping

PROVIDER: PRJEB41484 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4866750.fastq.gz	Fastqsanger.gz
	ERR4866760.fastq.gz	Fastqsanger.gz
	ERR4866770.fastq.gz	Fastqsanger.gz
	ERR4866751.fastq.gz	Fastqsanger.gz
	ERR4866761.fastq.gz	Fastqsanger.gz

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Identification of regulators of exit from naïve pluripotent state by enhancer trap integration site mapping

Project description:To identify regulators of exit from the naïve pluripotent state we performed an enhancer trap screen under sensitized conditions. Briefly, haploid mouse ESCs with a Puromycin resistance gene under the control of Oct4 regulatory elements were mutagenized using viruses harboring enhancer trap constructs and subjected to differentiation in the presence of 3uM CHIR with concomitant selection for Oct4 expression. Selected cells were harvested after 16, 20, and 23 days and the extracted genomic DNA, together with genomic DNA of cells taken before selection, subjected to inverse PCR and sequencing. This allowed for mapping of enhancer trap integration sites and identifying genes whose targeting is enriched during selection.

2021-07-07 | E-MTAB-9796 | biostudies-arrayexpress

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.

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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).

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Project description:Chromatin activity of IκBα mediates the exit from naïve pluripotency

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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]

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Project description:Defining how human pluripotent cell identity is controlled and in particular how naïve pluripotency is acquired during cell reprogramming is crucial for the future applications of pluripotent stem cells. However, the regulatory pathways of naïve cell reprogramming remain incompletely understood. Here, we used genome-wide CRISPR-Cas9 screening to identify novel regulators of primed to naïve pluripotent stem cell reprogramming, including genes that are essential for reprogramming and genes that normally impede reprogramming and whose targeted deletion led to enhanced reprogramming. Integrated analysis defined specific chromatin complexes and signalling pathways as critical regulators of naïve reprogramming, and were largely distinct from regulators of somatic cell reprogramming. Mechanistically, PRC1.3 and PRDM14 are jointly required to transcriptionally repress developmental and gene regulatory factors to ensure naïve cell reprogramming. Additionally, small molecule inhibitors of reprogramming impediments increased the efficiency of naïve cell reprogramming, and are of practical benefit that can improve on current reprogramming methods. Taken together, we have identified novel regulators controlling the establishment of naïve pluripotency in human cells, which will open up new ways to exploit the full potential of pluripotent stem cells. These results also provide new insights into mechanisms that destabilise and reconfigure cell identity during cell state transitions.

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