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Expression data from undifferentiated human ES cell line, khES3, grown using complete, methionine, leucine or lysine deprived media and ES cell derived endoderm

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE55285 | GEO | 2014/04/17

SECONDARY ACCESSION(S): PRJNA239199

REPOSITORIES: GEO

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Expression data from undifferentiated human ES cell line, khES3, grown using complete, methionine, leucine or lysine deprived media and ES cell derived endoderm

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-04-17 | E-GEOD-55285 | biostudies-arrayexpress

Expression data from undifferentiated human ES cell line, khES3 grown using complete, leucine or lysine deprived media

2014-04-17 | GSE55284 | GEO

Expression data from undifferentiated human ES cell line, khES3, grown using complete or methionine deprived media and ES cell derived endoderm

2014-04-17 | GSE55283 | GEO

Expression data from undifferentiated human ES cell line, khES3 grown using complete, leucine or lysine deprived media

Project description:In undifferentiated human ES cells, 48hr Leucine deprivation (delta Leu) or Lysine deprivation (delta Lys) led to apoptosis. We used microarrays to detail the mollecular mechanism of cell-death caused by Leu, Lys deprivation in undifferentiated ES cells. Cells were harvested at undifferentiated stages for RNA extraction and hybridization on Affymetrix microarrays. We performed gene expression profiles of undifferentiated khES3 cells cultured in complete (comple),Leu or Lys deprivation for 5 hr.

2014-04-17 | E-GEOD-55284 | biostudies-arrayexpress

Expression data from undifferentiated human ES cell line, khES3, grown using complete or methionine deprived media and ES cell derived endoderm

Project description:In undifferentiated human ES cells, 5hr Met deprivation (delta Met) led to decreased proliferation, and prolonged 24hr Met deprivation resulted in G0-G1 phase cell cycle arrest, which then led to apoptosis. We used microarrays to detail the molecular mechanism of cell-death caused by Met deprivation in undifferentiated ES cells and checked the difference of Met cycle relate gene expression between undifferentiated human ES cells and ES cell derived endoderm. Cells were harvested at undifferentiated or differentiated stages for RNA extraction and hybridization on Affymetrix microarrays. We performed gene expression profiles of undifferentiated khES3 cells cultured in complete (compl) or Met-deprived conditions (deltaMet) for 5 or 24 hr. And 0hr untreated cells and endoderm cells were used as a comparison

2014-04-17 | E-GEOD-55283 | biostudies-arrayexpress

Gata4 directs development of cardiac-inducing endoderm from ES cells.

Project description:The transcription factor Gata4 is essential for normal heart morphogenesis and regulates the survival, growth, and proliferation of cardiomyocytes. We tested if Gata4 can specify cardiomyocyte fate from an uncommitted stem or progenitor cell population, by developing a system for conditional expression of Gata4 in embryonic stem cells. We find that in embryoid body cultures containing even a low ratio of these cells, expression of Gata4 is sufficient to enhance significantly the generation of cardiomyocytes, via a non-cell-autonomous mechanism. The Gata4-expressing cells do not generate cardiac or other mesoderm derivatives. Rather, Gata4 expression directs the development of two types of Sox17+ endoderm. This includes an epCam+Dpp4+ subtype of visceral endoderm. In addition, Gata4 generates similar amounts of epCam+Dpp4- definitive endoderm enriched for Cxcr4, FoxA2, FoxA3, Dlx5 and other characteristic transcripts. Both types of endoderm express cardiac-inducing factors, including WNT antagonists Dkk1 and Sfrp5, although the visceral endoderm subtype has much higher cardiac-inducing activity correlating with relatively enhanced levels of transcripts encoding BMPs. The Gata4-expressing cells eventually express differentiation markers showing commitment to liver development, even under conditions that normally support mesoderm development. The results suggest that Gata4 is capable of specifying endoderm fates that facilitate, with temporal and spatial specificity, the generation of cardiomyocyte progenitors from associated mesoderm.

| S-EPMC2799892 | biostudies-literature

Gene expression comparison of human ES cells grown in different media

Project description:Mouse embryonic fibroblasts can be used to condition basis human ES cell medium to allow feeder-free growth. To investigate the impact of factors released by the MEFs on gene expression in hES cells, global gene expression was analysed in cells grown in MEF-conditioned medium as compared to cells grown in a chemically defined one. Keywords: Media comparison

2008-03-12 | GSE9094 | GEO

Sox7 is dispensable for primitive endoderm differentiation from mouse ES cells.

Project description:BackgroundPrimitive endoderm is a cell lineage segregated from the epiblast in the blastocyst and gives rise to parietal and visceral endoderm. Sox7 is a member of the SoxF gene family that is specifically expressed in primitive endoderm in the late blastocyst, although its function in this cell lineage remains unclear.ResultsHere we characterize the function of Sox7 in primitive endoderm differentiation using mouse embryonic stem (ES) cells as a model system. We show that ectopic expression of Sox7 in ES cells has a marginal effect on triggering differentiation into primitive endoderm-like cells. We also show that targeted disruption of Sox7 in ES cells does not affect differentiation into primitive endoderm cells in embryoid body formation as well as by forced expression of Gata6.ConclusionsThese data indicate that Sox7 function is supplementary and not essential for this differentiation from ES cells.

| S-EPMC4609079 | biostudies-literature

Pdx1 and Ngn3 overexpression enhances pancreatic differentiation of mouse ES cell-derived endoderm population.

Project description:In order to define the molecular mechanisms regulating the specification and differentiation of pancreatic β-islet cells, we investigated the effect of upregulating Pdx1 and Ngn3 during the differentiation of the β-islet-like cells from murine embryonic stem (ES) cell-derived activin induced-endoderm. Induced overexpression of Pdx1 resulted in a significant upregulation of insulin (Ins1 and Ins2), and other pancreas-related genes. To enhance the developmental progression from the pancreatic bud to the formation of the endocrine lineages, we induced the overexpression express of Ngn3 together with Pdx1. This combination dramatically increased the level and timing of maximal Ins1 mRNA expression to approximately 100% of that found in the βTC6 insulinoma cell line. Insulin protein and C-peptide expression was confirmed by immunohistochemistry staining. These inductive effects were restricted to c-kit(+) endoderm enriched EB-derived populations suggesting that Pdx1/Ngn3 functions after the specification of pancreatic endoderm. Although insulin secretion was stimulated by various insulin secretagogues, these cells had only limited glucose response. Microarray analysis was used to evaluate the expression of a broad spectrum of pancreatic endocrine cell-related genes as well as genes associated with glucose responses. Taken together, these findings demonstrate the utility of manipulating Pdx1 and Ngn3 expression in a stage-specific manner as an important new strategy for the efficient generation of functionally immature insulin-producing β-islet cells from ES cells.

| S-EPMC3172220 | biostudies-literature

Hi-C of WT E14 mouse ES cells grown in serum and 2i media

Project description:Dynamic reprogramming of global DNA methylation impacts on the genomic deposition of the Polycomb-mediated repressive histone mark H3K27me3. DNA hypomethylation in ground state embryonic stem cells (ESCs) results in a reversible redistribution of H3K27me3 from its normal target loci. Thus, a signalling induced shift of ESCs to ground state results in both DNA methylation and Polycomb patterns that are quite distinct from their primed counterparts. Here we investigated the impact of DNA methylation directed Polycomb redistribution on higher-order chromatin structure in the ground state. Using a targeted single-locus approach (FISH) we can demonstrate local decompaction at Hox loci in the ground state, which is consistent with genome-wide data (Hi-C) indicating that chromatin structure is globally altered in ground state relative to primed ESCs. Polycomb targets are similarly decompacted in hypomethylated E3.5 mouse blastocysts. ESC lines which maintain a high level of DNA methylation in ground state show no decompaction at Hox loci. Our results suggest that DNA-methylation mediated reprogramming of Polycomb binding drives higher order chromatin organisation in stem cells and early development.

2019-01-30 | GSE124342 | GEO

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