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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gata6 induced XEN-like cells w/o Sox7

ABSTRACT: To understand the role of Sox7 in primitive endoderm differentiation, we compare the gene expression pattern of Sox7 (+/-) and Sox7 (-/-) ES cells with or without dexamethasome (Dex) treatment. Because these ES cells harbour Gata6-GR transgene, Dex treatment forces ES cells differentate into XEN-like cells. As Sox7 (-/-) ES cells can differentiate into XEN-like cell by morphology, we assessed genome wide gene expression pattern. Sox7 (+/-) ES cells and Sox7 (-/-) ES cells are forced to differentiate into XEN-like cells by Gata6-GR transgene. To compare the gene expression, we collected RNA samples at day4 with or without dexamethasone treatment from each genotype.

ORGANISM(S): Mus musculus

SUBMITTER: Hitoshi Niwa

PROVIDER: E-GEOD-66971 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gata6 induced XEN-like cells w/o Sox7

Project description:To understand the role of Sox7 in primitive endoderm differentiation, we compare the gene expression pattern of Sox7 (+/-) and Sox7 (-/-) ES cells with or without dexamethasome (Dex) treatment. Because these ES cells harbour Gata6-GR transgene, Dex treatment forces ES cells differentate into XEN-like cells. As Sox7 (-/-) ES cells can differentiate into XEN-like cell by morphology, we assessed genome wide gene expression pattern.

2015-09-14 | GSE66971 | GEO

Sall4 regulates distinct transcription circuitries in different blastocyst-derived stem cell lineages

Project description:Stem cells self-renew or differentiate under the governance of a stem cell-specific transcriptional program with each transcription factor orchestrating the activities of a particular set of genes. Here we demonstrate that a single transcription factor is able to regulate distinct core circuitries in two different blastocyst-derived stem cell lines, embryonic stem (ES) and extra-embryonic endoderm (XEN) cells. The transcription factor, Sall4, is required for early embryonic development and for ES cell pluripotency. Sall4 is also expressed in XEN cells and depletion of Sall4 disrupts self-renewal and induces differentiation. Genome-wide analysis reveals Sall4 is regulating different gene sets in ES and XEN cells, and depletion of Sall4 targets in the respective cell types induces differentiation. With Oct4, Sox2 and Nanog, Sall4 forms a crucial interconnected auto-regulatory network in ES cells. In XEN cells, Sall4 regulates key XEN lineageassociated genes, Gata4, Gata6, Sox7 and Sox17. Our findings demonstrate how Sall4 functions as an essential stemness factor for two different stem cell lines. Keywords: ES/XEN comparison, ES Sall4 KD/control KD comparison, and XEN Sall4 KD/control KD comparison

2008-08-19 | GSE12482 | GEO

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

Mus musculus

Project description:Gata6 induced XEN-like cells w/o Sox7

| PRJNA278525 | ENA

Gata6 potently initiates reprogramming of pluripotent and differentiated cells to extraembryonic endoderm stem cells [ChIP-Seq & RNA-Seq]

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. (1) Microarray analysis of Gata6 overexpressing cells from 12 to 144 hours of doxycycline treatment in mouse embryonic stem (mES) cells compared to uninduced mES cells, embryo-derived XEN cells and Sox7 overexpressing mES cells after 144 hours of doxycycline treatment. (2) ChIP-seq analysis of Gata6 binding 36 hours following doxycycline treatment. (3) ChIP-seq analysis of Gata6 binding in embryo-derived XEN cells. (4) RNA-seq analysis of GATA6 overexpressing cells following 144 hours of induction in hES cells.

2015-06-30 | E-GEOD-69322 | biostudies-arrayexpress

Crosstalk between the glucocorticoid and mineralocorticoid receptor boosts glucocorticoid-induced killing of multiple myeloma cells

Project description:The glucocorticoid receptor (GR) is a crucial drug target in multiple myeloma as its activation with glucocorticoids effectively triggers myeloma cell death. However, as high-dose glucocorticoids are also associated with deleterious side effects, novel approaches are urgently needed to improve GR’s action in myeloma. Here we reveal a functional crosstalk between GR and the mineralocorticoid receptor (MR) that culminates in improved myeloma cell killing. We show that the GR agonist Dexamethasone (Dex) downregulates MR levels in a GR-dependent way in myeloma cells. Co-treatment of Dex with the MR antagonist Spironolactone (Spi) enhances Dex-induced cell killing in primary, newly diagnosed GC-sensitive myeloma cells, while in a relapsed GC-resistant setting, Spi alone induces distinct myeloma cell killing. On a mechanistic level, we find that a GR-MR crosstalk is arising from an endogenous interaction between GR and MR in myeloma cells. Quantitative dimerization assays show that Spi reduces Dex-induced GR-MR heterodimerization and completely abolishes Dex-induced MR MR homodimerization but leaves GR-GR homodimerization intact. Unbiased transcriptomics further reveals that c-myc and many of its target genes are downregulated most by Dex and Spi combined, while proteomics analyses identify that several metabolic hallmarks are modulated most by this combination treatment. Finally, we identified a subset of Dex+Spi downregulated genes and proteins that may predict prognosis in the CoMMpass patient cohort. Our study demonstrates that GR-MR crosstalk is therapeutically relevant in myeloma as it provides novel strategies towards glucocorticoid-based dose-reduction.

2023-10-24 | PXD043635 | Pride

Gene expression profiling in Vav-Etv2 KSL and Granulocyte hematopoietic cells

Project description:Etv2 transgene was expressed from ROSA26 locus by removing floxed STOP cassette by Vav Cre transgene. KSL or Mac1+/Gr1+ cells were sorted from control or Vav-Etv2 bone marrow and compared for gene expression in duplicate. This study will reveal the effect of Etv2 transgene in adult hematopoietic cells. The effect of Etv2 overexpression in relevant mouse tissue will be important to understand its effect in comparison with in ES cells. Genes aberrantly regulated by Etv2 overexpression will help to understand the caveat when using Etv2 to induce endothelial and hematopoietic cells in vitro. Sample ID #1;KSL;Control #2;KSL;Control #3;KSL;Tg #4;KSL;Tg #5;Gr;Control #6;Gr;Control #7;Gr;Tg #8;Gr;Tg

2012-05-09 | E-GEOD-36731 | biostudies-arrayexpress

Mus musculus

Project description:Mouse ES cells versus XEN cells

| PRJNA91333 | ENA

Essential functions of the Glucocorticoid Receptor require direct DNA binding [RNA-seq]

Project description:We performed RNA sequencing in Mouse Embryonic Fibroblasts (MEFs) of GR wild-type and GR Zn. Cells were treated with: vehicle (EtOH), Dexamethasone (Dex), Lipopolysaccharide (LPS) or Dex+LPS. We show that GR Zn does not regulate any GR target gene

2019-12-31 | GSE124919 | GEO

IRF2BP2 Modulates the Crosstalk between Glucocorticoid and TNF Signaling

Project description:Here we have analyzed the role of interferon regulatory factor-2 binding protein-2 (IRF2BP2) in glucocorticoid and tumor necrosis factor alpha (TNF) signaling. We used ChIP-seq to analyze chromatin binding of IRF2BP2 in glucocorticoid (dexamethasone, dex) and vehicle treated HEK293 cells expressing GR (HEK293-GR). Furthermore, we used RNA-seq to analyze how silencing of IRF2BP2 modulates transcriptional responses to dex treatment in HEK293-GR cells, and dex, TNF and co-treatment (dex and TNF, DT) in A549 cells.

2019-06-03 | GSE124636 | GEO

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