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GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [RNA-seq]

ABSTRACT: GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [RNA-seq]

PROVIDER: PRJNA656447 | ENA |

REPOSITORIES: ENA

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GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells.

Project description:GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells.

| PRJNA656438 | ENA

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [ATAC-seq]

Project description:Investigation of the role played by GATA6 in establishing the definitive endoderm chromatin accessbility profile. We used pluripotent stem cells as a model of early development. We derived GATA6-/- pluripotent cells with an inducible GATA6 construct that permits exongenous GATA6 cDNA expression upon supplmentation of doxycycline. We differentiated GATA6 +/+ and GATA6-/- (with and without doxycyline) cells to definitive endoderm and analyzed the chromatin profile using ATAC-seq.

2021-06-07 | GSE156018 | GEO

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [RNA-seq]

2021-06-07 | GSE156020 | GEO

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [ChIP-seq]

2021-06-07 | GSE156019 | GEO

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [TF_ChIP-seq]

Project description:Investigation of the role played by GATA6 in establishing the definitive endoderm chromatin accessbility profile. We used pluripotent stem cells as a model of early development. We derived GATA6-/- pluripotent cells with an inducible GATA6 or FOXA2 construct that permits exongenous GATA6 or FOXA2 cDNA expression upon supplementation of doxycycline. We differentiated GATA6+/+ and GATA6-/- (with and without doxycyline) cells to definitive endoderm and analyzed transcription factor binding profiles using CHIP-seq.

2021-06-07 | GSE164231 | GEO

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [TF_ChIP-seq]

Project description:GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [TF_ChIP-seq]

| PRJNA689593 | ENA

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [ATAC-seq]

Project description:GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [ATAC-seq]

| PRJNA656444 | ENA

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [ChIP-seq]

Project description:GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human induced pluripotent stem cells [ChIP-seq]

| PRJNA656448 | ENA

Gata6 potently initiates reprogramming of pluripotent and differentiated cells to extraembryonic endoderm stem cells [time-course microarray]

Project description:Transcription factor-mediated reprogramming is a powerful method to study cell fate changes. In this work, we demonstrate that the transcription factor Gata6 can initiate reprograming of multiple cell types to induced extraembryonic endoderm (iXEN) cells. Intriguingly, Gata6 is sufficient to drive iXEN cells from mouse pluripotent cells and differentiated neural cells. Furthermore, GATA6 induction in human ES (hES) cells also downregulates pluripotency gene expression and upregulates extraembryonic endoderm genes, revealing a conserved function in mediating this cell fate switch. Profiling transcriptional changes following Gata6 induction in mES cells reveals step-wise pluripotency factor disengagement, with initial repression of Nanog and Esrrb, then Sox2 and finally Oct4, alongside step-wise activation of extraembryonic endoderm genes. Chromatin immunoprecipitation and subsequent high-throughput sequencing analysis shows Gata6 enrichment near both pluripotency and endoderm genes, suggesting that Gata6 functions as both a direct repressor and activator. Together this demonstrates that Gata6 is a versatile and potent reprogramming factor that can act alone to drive a cell fate switch from diverse cell types. Time-course microarray analysis of Gata6-mediated reprogramming from 12 to 144 hours of doxycycline treatment in mouse embryonic stem (mES) cells compared to uninduced mES cells, embryo-derived extraembryonic endoderm (XEN) cells and Sox7 overexpressing mES cells after 144 hours of doxycycline treatment.

2015-06-30 | E-GEOD-69321 | biostudies-arrayexpress

GATA6-AS1 Regulates GATA6 Expression to Modulate Human Endoderm Differentiation

Project description:Transcriptome analysis has uncovered a series of long noncoding RNAs (lncRNAs) transcribed during cell differentiation. Here, we uncovered lncRNA GATA6-AS1 is a functional lncRNA in definitive endoderm (DE) differentiation. We found GATA6-AS1 positively regulated the expression of endoderm key factor GATA6, which was different from previous reports in other biological contexts. Further investigation showed GATA6-AS1 interacted with SMAD2/3 and recruited SMAD2/3 to the promoter region of the GATA6 gene locus. In addition, overexpression of GATA6 was able to rescue the defect of DE differentiation due to the absence of GATA6-AS1, suggesting GATA6 was the functional target of GATA6-AS1 during endoderm differentiation. Ultimately, our study uncovers GATA6-AS1 is necessary for DE and pancreas differentiation, and reveals the detailed regulation mechanism between GATA6-AS1 and DE differentiation.

2020-07-26 | GSE143499 | GEO

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