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Expression data from embryonic stem cells differentiation

ABSTRACT: Pluripotency-associated transcription factor Foxd3 is required for maintaining pluripotent cells. However, the molecular mechanisms underlying its function are largely unknown. Here, we report that Foxd3 maintains the ESC identity through counteracting differentiation induction of Calcienurin-NFAT signaling. We used microarrays to detail the global programme of gene expression underlying overexpression of Foxd3 and NFATc3 in ESCs or deletion of Foxd3 in ESCs Total RNA was extracted from the mESCs under the following conditions:1) a control group transfected with an empty vector; a Foxd3 overexpression group; a NFATc3 overexpression group and a combination group with Foxd3 and NFATc3 overexpression 2) Foxd3fl/fl:Cre-ERT cells treated with Tamoxifen for 0 day and 2 days.

ORGANISM(S): Mus musculus

SUBMITTER: Shiyue Zhang

PROVIDER: E-GEOD-58960 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Foxd3 suppresses NFAT-mediated differentiation to maintain self-renewal of embryonic stem cells.

Zhu Lili L Zhang Shiyue S Jin Ying Y

EMBO reports 20141106 12

Pluripotency-associated transcription factor Foxd3 is required for maintaining pluripotent cells. However, molecular mechanisms underlying its function are largely unknown. Here, we report that Foxd3 suppresses differentiation induced by calcineurin-NFAT signaling to maintain the ESC identity. Mechanistically, Foxd3 interacts with NFAT proteins and recruits co-repressor Tle4, a member of the Tle repressor family highly expressed in undifferentiated ESCs, to suppress NFATc3's transcriptional acti ...[more]

PMID: 25378483

Similar Datasets

Expression data from embryonic stem cells differentiation

Project description:Pluripotency-associated transcription factor Foxd3 is required for maintaining pluripotent cells. However, the molecular mechanisms underlying its function are largely unknown. Here, we report that Foxd3 maintains the ESC identity through counteracting differentiation induction of Calcienurin-NFAT signaling. We used microarrays to detail the global programme of gene expression underlying overexpression of Foxd3 and NFATc3 in ESCs or deletion of Foxd3 in ESCs

2014-08-18 | GSE58960 | GEO

MS-based quantitative proteomic analysis of embryonic stem cells with normal and reduced expression of Rsl24d1.

Project description:Embryonic stem cell (ESC) fate decisions are regulated by a complex molecular circuitry that requires tight and coordinated gene expression regulations at multiple levels from chromatin organization to mRNA processing. Recently, ribosome biogenesis and translation have emerged as key pathways that efficiently control stem cell homeostasis. However, the molecular mechanisms underlying the regulation of these pathways remain largely unknown to date. Here, we analyzed the expression, in mouse ESCs, of over 300 genes involved in ribosome biogenesis and we identified RSL24D1 as the most differentially expressed between self-renewing and differentiated ESCs. RSL24D1 is highly expressed in multiple mouse pluripotent stem cell models and its expression profile is conserved in human ESCs. RSL24D1 is associated with nuclear pre-ribosomes and is required for the maturation and the synthesis of 60S subunits in mouse ESCs. Interestingly, RSL24D1 depletion significantly impairs global translation, particularly of key pluripotency factors, including POU5F1 and NANOG, as well as components of the polycomb repressive complex 2 (PRC2). Consistently, RSL24D1 is required for mouse ESC self-renewal and proliferation. Taken together, we show that RSL24D1-dependant ribosome biogenesis is required to both sustain the expression of pluripotent transcriptional programs and silence developmental programs, which concertedly dictate ESC homeostasis.

2023-01-10 | PXD030497 | Pride

Foxd3 binding at enhancers controls developmental timing of gene expression by regulation of histone acetylation [ChIP-seq]

Project description:Transcription factor/enhancer interactions determine cell specific gene expression. Here, we followed enhancers during differentiations of embryonic stem (ESCs) to epiblast like cells (EpiLCs). There were highly dynamic changes in histone lysine 27 acetylation at enhancer sites throughout the genome. These sites were enriched for a Foxd3 binding motif, a forkhead transcription factor essential in early embryonic development. Surprisingly, Foxd3 occupied largely mutually exclusive sites in the ESCs versus EpiLCs. Foxd3 bound to nucleosome occupied regions, simultaneously evicting the histones while inhibiting full gene expression through the recruitment of histone deacetylases. Knockout of Foxd3 resulted in hyperacetylation and transcriptional upregulation of neighboring genes, many of which were further upregulated at later stages of differentiation. These data show that Foxd3 primes enhancer sites during pregastrulation by removing nucleosomes, yet suppresses neighboring histone hyperacetylation. Such a mechanism may be common to many transcription factors that prepare enhancers for later gene activation during development. ChIP-seq of H3K4me1, H3K27ac, H3K27me3, p300, H3K4me3, RNA Pol2 and Oct4 in four pluripotent states: embryonic stem cells (ESCs) day 1 ESC differentiation, Epi-like stem cells (EpiLCs), and epiblast stem cells (EpiSCs); ChIP-seq of 3XFlag tagged Foxd3 in ESCs and EpiLCs; ChIP-seq of H3K4me1, H3K27ac, H3K27me3, p300 and H3K4me3 in Foxd3 conditional knockout cells (tamoxifen-inducible) -/+ 36h Tamoxifen treatemnt. ChIP seq of Flag-Foxd3 (third replicate), ChIP-seq of HDAC1 and Brg1 in WT and Foxd3 KO cells and MNase-ChIP-seq of H3K4me1

2015-12-08 | E-GEOD-58407 | biostudies-arrayexpress

Foxd3 binding at enhancers controls developmental timing of gene expression by regulation of histone acetylation [expression array]

Project description:Transcription factor/enhancer interactions determine cell specific gene expression. Here, we followed enhancers during differentiations of embryonic stem (ESCs) to epiblast like cells (EpiLCs). There were highly dynamic changes in histone lysine 27 acetylation at enhancer sites throughout the genome. These sites were enriched for a Foxd3 binding motif, a forkhead transcription factor essential in early embryonic development. Surprisingly, Foxd3 occupied largely mutually exclusive sites in the ESCs versus EpiLCs. Foxd3 bound to nucleosome occupied regions, simultaneously evicting the histones while inhibiting full gene expression through the recruitment of histone deacetylases. Knockout of Foxd3 resulted in hyperacetylation and transcriptional upregulation of neighboring genes, many of which were further upregulated at later stages of differentiation. These data show that Foxd3 primes enhancer sites during pregastrulation by removing nucleosomes, yet suppresses neighboring histone hyperacetylation. Such a mechanism may be common to many transcription factors that prepare enhancers for later gene activation during development. Total RNA obtained Foxd3 knockout embryonic stem cells (ESCs) and epiblast-like cells (EpiLCs) (treated with 1uM tamoxifen for 36h to induce knockout) compared to wild-type controls

2015-12-08 | E-GEOD-58317 | biostudies-arrayexpress

Quantitative subcellular proteomics using SILAC reveals enhanced metabolic buffering in ground state pluripotency

Project description:The ground state of pluripotency is defined as a minimal unrestricted state as present in the Inner Cell Mass (ICM). Mouse embryonic stem cells (ESCs) grown in a defined serum-free medium with two kinase inhibitors (‘2i’) reflect this state, whereas ESCs grown in the presence of serum (‘serum’) share more similarities with post implantation epiblast cells. Pluripotency results from an intricate interplay between cytoplasmic, nuclear and chromatin-associated proteins. Therefore, quantitative information on the (sub)cellular proteome is essential to gain insight in the molecular mechanisms driving different pluripotent states. Here, we describe a full SILAC workflow and quality controls for proteomic comparison of 2i and serum ESCs. We demonstrate that this workflow is applicable for subcellular proteomics of the cytoplasm, nuclear and chromatin. The obtained quantitative information revealed increased levels of naïve pluripotency factors on the chromatin of 2i ESCs. Further, we demonstrate that these pluripotent states are supported by distinct metabolic programs, which include upregulation of free radical buffering by the glutathione pathway in 2i ESCs. Through induction of intracellular radicals, we show that the altered metabolic environment renders 2i ESCs less sensitive to oxidative stress. Altogether, this work provides novel insights into the proteome landscape underlying ground state pluripotency.

2018-11-07 | PXD009217 | Pride

Temporal RNA-seq expression profiling of Sox17-medaited XEN conversion of ESCs

Project description:The transcription factor Sox17 is expressed in early primitive endoderm-fated cells of the mouse embryo and in embryo-derived extraembryonic endoderm (ExEn) stem (XEN) cells. We have shown that overexpression of Sox17 in mouse embryonic stem cells (ESCs) drives cell fate to a committed XEN-like cell state (Sox17-XEN cells). When placed back into the embryo, Sox17-XEN cells contribute exclusively to the ExEn. Transient Sox17 expression is sufficient to drive this fate change during which time cells transit through distinct intermediate states prior to the generation of functional XEN-like cells. We identified dynamic regulatory networks driving Sox17-mediated XEN conversion by analyzing a dynamic regulatory map of gene expression bifurcation points throughout conversion, created using RNA-seq time series data. We found that Sox17 orchestrates this conversion process by acting in autoregulatory and feed-forward network motifs, regulating dynamic gene regulatory networks (GRNs) directing cell fate. We have shown that Sox17-mediated XEN conversion provides a powerful tool for understanding the regulation of cell fate changes and for the elucidation of GRNs regulating lineage decisions in the mouse embryo. Total RNA was extracted during a time course of Sox17 overexpression in mouse ESCs at 7 time points as well as from wild-type ESCs and wild-type XEN cells.

2014-09-05 | E-GEOD-61102 | biostudies-arrayexpress

Foxd3 binding at enhancers controls developmental timing of gene expression by regulation of histone acetylation [ChIP-seq]

2015-12-08 | GSE58407 | GEO

Foxd3 binding at enhancers controls developmental timing of gene expression by regulation of histone acetylation [expression array]

2015-12-08 | GSE58317 | GEO

FungenES: FunGenES_UKOE-4: Functional characterization and transcriptome analysis of embryonic stem cells-derived contractile smooth muscle cells

Project description:This experiment is part of the FunGenES project (FunGenES - Functional Genomics in Embryonic Stem Cells partially funded by the 6th Framework Programme of the EuropeanUnion, http://www.fungenes.org). The experiment was conducted at University of Cologne, Cologne, Germany. Goal of the experiment is a complete transcriptome profiling of contractile smooth muscle cells (SMCs) differentiated from embryonic stem cells which is crucial for the characterization of smooth muscle gene expression signatures and will contribute to defining biological and physiological processes in these cells. We have generated a transgenic embryonic stem cell line expressing both the puromycin acetyl transferase and enhanced green fluorescent protein cassettes under the control of the Acta2 promoter.This experiment allows the identification of specific biological and physiological processes in the contractile phenotype SMCs and will contribute to the understanding of these processes in early SMCs derived from embryonic stem cells.

2011-02-25 | E-TABM-1123 | biostudies-arrayexpress

Systematic Identification of Defined Conditions for Induction and Maintenance of Naive Human Pluripotency [expression]

Project description:Embryonic stem cells (ESCs) of mice and humans have distinct molecular and biological characteristics, raising the question whether an earlier ‘naive’ state of pluripotency may exist in humans. Here we took a systematic approach to identify small molecules that support autonomous self-renewal of naive human ESCs based on maintenance of endogenous OCT4 distal enhancer activity, a molecular signature of ground state pluripotency. Iterative chemical screening identified a combination of five kinase inhibitors that induces and maintains OCT4 distal enhancer activity when applied directly to conventional human ESCs. These inhibitors generate a homogeneous population of human pluripotent stem cells in which transcription factors associated with the ground state of pluripotency are highly upregulated. Comparison with previously reported naive human ESCs indicates that our kinase inhibitor cocktail captures a novel pluripotent state in humans that closely resembles mouse ESCs. Expression analysis was performed on two groups of human ESC samples: WIBR2 (P12 and P14), WIBR3 (P9) and WIN1 (P10) human ESCs derived in our optimized naive medium (5i/L/A or 6i/L/A, as indicated), and parental WIBR2 and WIBR3 human ESCs in primed human ESC medium.

2014-07-16 | E-GEOD-59430 | biostudies-arrayexpress

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