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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE162581 | GEO | 2021/08/06

REPOSITORIES: GEO

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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]

2021-08-06 | GSE162579 | GEO

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

2021-08-06 | GSE162578 | GEO

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]

| PRJNA682242 | ENA

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

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

| PRJNA682243 | ENA

The ETS transcription factor ERF controls the exit from the naive pluripotent state in a MAPK-dependent manner.

Project description:The naïve epiblast transitions to a pluripotent primed state during embryo implantation. Despite the relevance of the FGF pathway during this period, little is known about the downstream effectors regulating this signaling. Here, we examined the molecular mechanisms coordinating the naïve to primed transition by using inducible ESC to genetically eliminate all RAS proteins. We show that differentiated RASKO ESC remain trapped in an intermediate state of pluripotency with naïve-associated features. Elimination of the transcription factor ERF overcomes the developmental blockage of RAS-deficient cells by naïve enhancer decommissioning. Mechanistically, ERF regulates NANOG expression and ensures naïve pluripotency by strengthening naïve transcription factor binding at ESC enhancers. Moreover, ERF negatively regulates the expression of the methyltransferase DNMT3B, which participates in the extinction of the naïve transcriptional program. Collectively, we demonstrated an essential role for ERF controlling the exit from naïve pluripotency in a MAPK-dependent manner during the progression to primed pluripotency.

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Ets transcription factor GABP controls T cell homeostasis and immunity.

Project description:Peripheral T cells are maintained in the absence of vigorous stimuli, and respond to antigenic stimulation by initiating cell cycle progression and functional differentiation. Here we show that depletion of the Ets family transcription factor GA-binding protein (GABP) in T cells impairs T-cell homeostasis. In addition, GABP is critically required for antigen-stimulated T-cell responses in vitro and in vivo. Transcriptome and genome-wide GABP-binding site analyses identify GABP direct targets encoding proteins involved in cellular redox balance and DNA replication, including the Mcm replicative helicases. These findings show that GABP has a nonredundant role in the control of T-cell homeostasis and immunity.

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hnRNPLL controls pluripotency exit of embryonic stem cells by modulating alternative splicing of Tbx3 and Bptf.

Project description:The regulatory circuitry underlying embryonic stem (ES) cell self-renewal is well defined, but how this circuitry is disintegrated to enable lineage specification is unclear. RNA-binding proteins (RBPs) have essential roles in RNA-mediated gene regulation, and preliminary data suggest that they might regulate ES cell fate. By combining bioinformatic analyses with functional screening, we identified seven RBPs played important roles for the exit from pluripotency of ES cells. We characterized hnRNPLL, which mainly functions as a global regulator of alternative splicing in ES cells. Specifically, hnRNPLL promotes multiple ES cell-preferred exon skipping events during the onset of ES cell differentiation. hnRNPLL depletion thus leads to sustained expression of ES cell-preferred isoforms, resulting in a differentiation deficiency that causes developmental defects and growth impairment in hnRNPLL-KO mice. In particular, hnRNPLL-mediated alternative splicing of two transcription factors, Bptf and Tbx3, is important for pluripotency exit. These data uncover the critical role of RBPs in pluripotency exit and suggest the application of targeting RBPs in controlling ES cell fate.

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