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C-Jun impedes somatic cell reprogramming by activating mesenchymal core regulators and suppressing pluripotent ones

ABSTRACT: The somatic cell fate can be converted to tumor or pluripotent ones by ectopic expression of transcription factors in vitro and in vivo. Many oncogenic transcription factors are known to mediate both fates as they share similar proliferative and metabolic properties. Paradoxically, we found c-Jun as the first oncogene that appears to specify a somatic fate, oppose the pluripotent one and impede reprogramming. We performed a series of high through out sequencing to understand the way cJun works.

ORGANISM(S): Mus musculus

PROVIDER: GSE50776 | GEO | 2015/06/10

SECONDARY ACCESSION(S): PRJNA218916

REPOSITORIES: GEO

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c-Jun impedes somatic cell reprogramming by activating mesenchymal core regulators and suppressing pluripotent ones

Project description:The somatic cell fate can be converted to tumor or pluripotent ones by ectopic expression of transcription factors in vitro and in vivo. Many oncogenic transcription factors are known to mediate both fates as they share similar proliferative and metabolic properties. Paradoxically, we found c-Jun as the first oncogene that appears to specify a somatic fate, oppose the pluripotent one and impede reprogramming. We performed a series of high through out sequencing to understand the way cJun works. To understand how c-Jun drives mESCs differentiating, we obtained c-Jun TetOn mESCs, and performed RNAseq 36h later with dox inducing or not . To understand why c-Jun blocks reprogramming while c-JunDN and Jdp2 can replace Oct4, we overexpressed these factors with KSM during reprogramming and performed RNAseq 3 Days after virus transfection. Moreover, to extend understand how these factors regulate gene expression, we also overexpressed these factors in MEF and performed RNAseq. Further more, to understand how cJun regulates cell fates and gene expression, we overexpressed c-Jun in mouse ESC and performed ChIP-seq. Also, we performed c-JunDN ChIP-seq during somatic cells reprogramming on day 3, to explore the binding sites of c-JunDN.

2015-06-10 | E-GEOD-50776 | biostudies-arrayexpress

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

Polycomb Repressive Complex 2 Restricts Human Naive Pluripotent Stem Cell to Trophoblast Fate Induction

Project description:Human naive pluripotent stem cells have unrestricted lineage potential. Underpinning this property, naive cells are thought to lack chromatin-based lineage barriers. However, this assumption has not been tested. Here, we apply multi-omics to comprehensively define the chromatin-associated proteome, histone post-translational modifications and transcriptome of human naive and primed pluripotent stem cells. Integrating the chromatin-bound proteome and histone modification data sets reveals differences in the relative abundance and activities of distinct chromatin modules, identifying a strong enrichment of Polycomb Repressive Complex 2 (PRC2)-associated H3K27me3 in naive pluripotent stem cell chromatin. Single-cell approaches and human blastoid models reveal that PRC2 activity acts as a chromatin barrier restricting the differentiation of naive cells towards the trophoblast lineage, and inhibiting PRC2 promotes trophoblast fate induction and cavity formation. Our results establish that human naive pluripotent stem cells are not epigenetically unrestricted, but instead possess chromatin mechanisms that oppose the induction of alternative cell fates.

2022-05-06 | PXD028111 | Pride

Integrated Multi-Omics Reveal Polycomb Repressive Complex 2 Restricts Human Trophoblast Induction

Project description:Human naive pluripotent stem cells have unrestricted lineage potential. Underpinning this property, naive cells are thought to lack chromatin-based lineage barriers. However, this assumption has not been tested. Here, we define the chromatin-associated proteome, histone post-translational modifications and transcriptome of human naive and primed pluripotent stem cells. Our integrated analysis reveals differences in the relative abundance and activities of distinct chromatin modules. We identify a strong enrichment of Polycomb Repressive Complex 2 (PRC2)-associated H3K27me3 in naive pluripotent stem cell chromatin, and H3K27me3 enrichment at promoters of lineage-determining genes, including trophoblast regulators. PRC2 activity acts as a chromatin barrier restricting the differentiation of naive cells towards the trophoblast lineage, while inhibition of PRC2 promotes trophoblast fate induction and cavity formation in human blastoids. Together, our results establish that human naive pluripotent stem cells are not epigenetically unrestricted, but instead possess chromatin mechanisms that oppose the induction of alternative cell fates.

2022-05-09 | PXD032792 | Pride

Integrated Multi-Omics Reveal Polycomb Repressive Complex 2 Restricts Human Trophoblast Induction

2022-05-06 | PXD028162 | Pride

H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States

Project description:H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States

| PRJNA818169 | ENA

SS18/BAFs regulate chromatin accessibility dynamics during pluripotent-somatic transition

Project description:The exit from pluripotency or pluripotent-somatic transition (PST) landmarks an event of mammalian development, and is also a representative cell-fate transition model, but remains largely unresolved. Recently, we reported construction of robust JUN-induced PST completed in one cell cycle and whose dominant regulator SS18/BAFs (Brg1/Brahma-associated factors). However, the transition process in the chromatin architecture and the roles played by BAF are still unknown. Here we report the dynamic changes of chromatin accessibility during JUN-induced PST. Meanwhile, SS18/BAFs mediates PST process by relocating from pluripotent loci to AP-1 associated ones and once compromised, JUN fails to open chromatin and PST will be delayed. Furthermore, we show that the relocation of SS18/BAF partially relays on histone modification H3K27ac, instead of JUN-centric protein-protein interaction. These results reveal the orchestration of master transcription factor, epigenetic machine, and histone modification in the cell fate transition.

2021-10-22 | PXD029277 |

Tox4 Modulates Cell Fate Reprogramming

Project description:Reprogramming to induced pluripotency induces the switch of somatic cell identity to induced pluripotent stem cells (iPSCs). However, the mediators and mechanisms of reprogramming remain largely unclear. To elucidate the mediators and mechanisms of reprogramming, we used a siRNA mediated knockdown approach for selected candidate genes during the conversion of somatic cells into iPSCs. We identified Tox4 as a novel factor that modulates cell fate, using reprogramming efficiency towards iPSCs as an assay. We found that Tox4 is needed early in reprogramming to efficiently generate early reprogramming intermediates, irrespective of reprogramming conditions used. Tox4 enables proper exogenous reprogramming factor expression and the closing and opening of putative somatic and pluripotency enhancers early during reprogramming, respectively. We show that TOX4 protein assembles into a high molecular form. Moreover, Tox4 is also required for the efficient conversion of fibroblasts towards the neuronal fate, suggesting a broader role of Tox4 in modulating cell fate. Our study reveals Tox4 as a novel transcriptional modulator of cell fate that mediates reprogramming from the somatic state to the pluripotent and neuronal fate.

2019-09-19 | GSE127932 | GEO

Tox4 Modulates Cell Fate Reprogramming

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Cell Fate Control by Engineered Chromatin Regulator

Project description:MS analysis to provide insights into proteins bound to engineered cell fate regulator NanogBiD during somatic cell reprogramming

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