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Jun-mediated changes in cell adhesion contribute to embryonic stem cell exit from ground state pluripotency

ABSTRACT: Jun-mediated changes in cell adhesion contribute to embryonic stem cell exit from ground state pluripotency

PROVIDER: PRJEB11808 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1141940.fastq.gz	Fastqsanger.gz
	ERR1141941.fastq.gz	Fastqsanger.gz
	ERR1141942.fastq.gz	Fastqsanger.gz
	ERR1141933.fastq.gz	Fastqsanger.gz
	ERR1141943.fastq.gz	Fastqsanger.gz

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Jun-mediated changes in cell adhesion contribute to embryonic stem cell exit from ground state pluripotency

Project description:Embryonic stem cells (ESC) are able to give rise to any somatic cell type. A lot is known about how ESC pluripotency is maintained, but comparatively less is known about how differentiation is promoted. Cell fate decisions are regulated by interactions between signalling and transcriptional networks. Recent studies have shown that the overexpression or downregulation of the transcription factor Jun can affect the ESC fate. Here we have focussed on the role of the Jun in the exit of mouse ESCs from ground state pluripotency and the onset of early differentiation. Transcriptomic analysis of differentiating ESCs reveals that Jun is required to upregulate a programme of genes associated with cell adhesion as ESCs exit the pluripotent ground state.

2015-12-07 | E-MTAB-4068 | biostudies-arrayexpress

Jun-Mediated Changes in Cell Adhesion Contribute to Mouse Embryonic Stem Cell Exit from Ground State Pluripotency.

Project description: Not available

| S-EPMC4864893 | biostudies-literature

Genome-scale screens identify JNK/JUN signaling as a barrier for pluripotency exit and endoderm differentiation

Project description:Human embryonic and induced pluripotent stem cells (hESCs/hiPSCs) hold great promise for cell-based therapies and drug discovery. However, homogeneous differentiation remains a major challenge, highlighting the need for understanding developmental mechanisms. We performed genome-scale CRISPR screens to uncover regulators of definitive endoderm (DE) differentiation, which unexpectedly uncovered five JNK/JUN family genes as key barriers of DE differentiation. The JNK/JUN pathway does not act through directly inhibiting the DE enhancers. Instead JUN co-occupies ESC enhancers with OCT4, NANOG and SMAD2/3, and specifically inhibits the exit from the pluripotent state by impeding the decommissioning of ESC enhancers and inhibiting the reconfiguration of SMAD2/3 chromatin binding from ESC to DE enhancers. Therefore, the JNK/JUN pathway safeguards pluripotency from precocious DE differentiation. Direct pharmacological inhibition of JNK significantly improves the efficiencies of generating DE and DE-derived pancreatic and lung progenitor cells, highlighting the potential of harnessing the knowledge from developmental studies for regenerative medicine.

2019-03-18 | GSE109524 | GEO

CHRAC/ACF Contribute to the Repressive Ground State of Chromatin

Project description:CHRAC/ACF Contribute to the Repressive Ground State of Chromatin

| PRJNA417803 | ENA

CHRAC/ACF Contribute to the Repressive Ground State of Chromatin [Mnase-seq]

Project description:CHRAC/ACF Contribute to the Repressive Ground State of Chromatin [Mnase-seq]

| PRJNA417813 | ENA

CHRAC/ACF Contribute to the Repressive Ground State of Chromatin [RNA-seq]

Project description:CHRAC/ACF Contribute to the Repressive Ground State of Chromatin [RNA-seq]

| PRJNA417814 | ENA

p110α of PI3K is Indispensable for Quiescence Exit in Adult Muscle Satellite Cells

Project description:Adult muscle stem cells (MuSC) are quiescent with a localization between myofibers and basal lamina. Upon injury, MuSC exit quiescence, reenter cell cycle, expand and differentiate for muscle regeneration. By using genetic mouse model, we identified p110α/mTORC1 signaling as a indispensable pathway that permits quiescence exit and cell cycle reentry. In order to dig out the downstream effectors, we compared the transcriptome of freshly isolated MuSC from Ctrl (p110α-f/+:R26-YFP/YFP:Pax7-CreER/CreER) to MuSC-specific p110α-null (iKO, p110α-f/f:R26-YFP/YFP:Pax7-CreER/CreER) mice by RNA-sequencing, and AP1 target genes were dramatically down-regulated in iKO MuSC. Restoration of Jun could significantly rescue the cell cycle reentry defect in iKO MuSC. In summary, we provided a p110α/mTORC1/Jun axis required for quiecence exit and cell cycle reentry of MuSC.

2018-02-25 | GSE109472 | GEO

Genome-wide maps of H3K27ac, H3K4me1, JUN and p-JUN in JUN overexpressed or JUN inactivated fibroblasts

Project description:To further dissect whether and how activated JUN reconfigures the chromatin landscape, we performed Chromatin Immunoprecipitation (ChIP)-seq analyses for H3K4me1 and H3K27ac. Based on the significant increase of H3K27ac levels at H3K4me1+ sites, we identified 3,017 JUN-activated enhancers in JUN WT cells. In contrast, JUN AA fails to significantly induce H3K27ac accumulation at these regions. Their enrichment levels at JUN-activated enhancers were significantly decreased after JNKi treatment. Besides, these enhancers are directly driven by JUN, especially phosphorylated JUN.

2022-12-09 | GSE196345 | GEO

CHRAC/ACF Contribute to the Repressive Ground State of Chromatin [RNA-seq]

Project description:The chromatin remodeling complexes CHRAC and ACF combine the ATPase ISWI with the signature subunit ACF1. These enzymes catalyze well-studied nucleosome sliding reactions in vitro, but how their actions affect physiological gene expression is unclear. Here we explored the influence of Drosophila CHRAC/ACF on transcription by complementary gain- and loss-of-function approaches. Targeting ACF1 to multiple reporter genes inserted at many different genomic locations revealed a context-dependent inactivation of poorly transcribed reporters in repressive chromatin. Accordingly, single-embryo transcriptome analysis of a Acf knock-out allele showed that only lowly expressed genes are de-repressed in the absence of ACF1. Finally, the nucleosome arrays in Acf-deficient chromatin show loss of physiological regularity, particularly in transcriptionally inactive domains. Taken together our results highlight that ACF1-containing remodeling factors contribute to the establishment of an inactive ground state of the genome through chromatin organization.

2018-02-05 | GSE106732 | GEO

CHRAC/ACF Contribute to the Repressive Ground State of Chromatin [Mnase-seq]

2018-02-05 | GSE106731 | GEO