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The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [Cut&Run]

ABSTRACT: The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [Cut&Run]

PROVIDER: PRJNA682243 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13188236_1.fastq.gz	Fastqsanger.gz
	SRR13188236_2.fastq.gz	Fastqsanger.gz
	SRR13188237_1.fastq.gz	Fastqsanger.gz
	SRR13188237_2.fastq.gz	Fastqsanger.gz
	SRR13188238_1.fastq.gz	Fastqsanger.gz

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The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [RRBS]

Project description:The naïve epiblast undergoes a transition to a pluripotent primed state during embryo implantation. Interestingly, a distinct intermediate stage during the naïve-to-primed transition has been recently described, the rosette stage. We propose the transcriptional repressor ERF as the MAPK-dependent switch that controls the exit from the rosette-stage of pluripotency. By using inducible ESC to genetically eliminate all RAS proteins, we show that, while differentiated RasKO ESC are reminiscent of the pluripotent rosette-stage, the absence of ERF overcomes the developmental blockage of RAS-deficient cells from this intermediate state. RNAseq data revealed that deletion of ERF restored the overall gene expression profile to a wild-type level in differentiated RasKO ESC. Mechanistically, ERF ensures naïve pluripotency by strengthening naïve pluripotent transcription factor binding and accessibility at specific ESC enhancers. Moreover, ERF regulates negatively the expression of the DNMT3 de novo methylases, which are essential for the extinction of the naïve transcriptional program. Our data revealed an essential role for ERF in the exit from rosette pluripotency as a regulator of the progression to primed pluripotency.

2021-08-06 | GSE162580 | GEO

The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [RNAseq]

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The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [Cut&Run]

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The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency.

Project description:The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency.

| PRJNA682237 | ENA

The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [RRBS]

Project description:The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [RRBS]

| PRJNA682241 | ENA

The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [RNAseq]

Project description:The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency [RNAseq]

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The ETS Transcription Factor ERF Controls the Exit from the Embryonic Rosette-stage of Pluripotency.

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

2021-08-06 | GSE162581 | GEO

Loss of Function Mutations in ETS2 Repressor Factor (ERF) Reveal a Balance Between Positive and Negative ETS Factors Controlling Prostate Oncogenesis [22PC RNA-seq]

Project description:Half of prostate cancers are caused by a gene-fusion that enables androgens to drive expression of the normally silent ETS transcription factor ERG in luminal prostate cells1-4. Recent prostate cancer genomic landscape studies5-10 have reported rare but recurrent point mutations in the ETS repressor ERF11. Here we show these ERF mutations cause decreased protein stability and ERF mutant tumours are mostly exclusive from those with ERG fusions. ERF loss recapitulates the morphologic and phenotypic features of ERG gain in primary mouse prostate tissue, including expansion of the androgen receptor (AR) transcriptional repertoire, and ERF has tumour suppressor activity in the same genetic background of PTEN loss that yields oncogenic activity by ERG. Furthermore, in a human prostate cancer model of ERG gain and wild-type ERF, ChIP-seq studies indicate that ERG inhibits the ability of ERF to bind DNA at consensus ETS sites. Consistent with a competition model, ERF loss rescues ERG-positive prostate cancer cells from ERG dependency. Collectively, these data provide evidence that the oncogenicity of ERG is mediated, in part, by displacement of ERF and raise the larger question of whether other gain-of-function oncogenic transcription factors might also inactivate endogenous tumour suppressors.

2017-06-08 | GSE83649 | GEO

Loss of Function Mutations in ETS2 Repressor Factor (ERF) Reveal a Balance Between Positive and Negative ETS Factors Controlling Prostate Oncogenesis [Organoids ChIP-Seq]

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Loss of Function Mutations in ETS2 Repressor Factor (ERF) Reveal a Balance Between Positive and Negative ETS Factors Controlling Prostate Oncogenesis [VCaP RNA-Seq]

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