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Unknown,Transcriptomics,Genomics,Proteomics

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3' RNA-Seq (3'SEQ) analysis gene expression profiling at G1-S transition in human embryonic stem cells (hESCs) and hESC-derived endoderm cells

ABSTRACT: In this report, we examine transcripts on a genome-wide level between the synchronized cell cycles of hESCs and hESC-derived endoderm cells. We found 10347, 10299 and 10362 genes expressed in the G1, G1/S, and S phase of hESCs, respectively; 10333, 10227 and 10215 genes expressed at the G1, G1/S and S phase of derived endoderm. We compared the transcriptome between these data sets and identified genes with differentiated phase expression between hESCs and hESC-derived endoderm cells. Examination of the transcriptome at the G1-S transition in hESCs compared to hESC-derived endoderm cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Edward Chuong

PROVIDER: E-GEOD-47117 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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3' RNA-Seq (3'SEQ) analysis gene expression profiling at G1-S transition in human embryonic stem cells (hESCs) and hESC-derived endoderm cells

Project description:In this report, we examine transcripts on a genome-wide level between the synchronized cell cycles of hESCs and hESC-derived endoderm cells. We found 10347, 10299 and 10362 genes expressed in the G1, G1/S, and S phase of hESCs, respectively; 10333, 10227 and 10215 genes expressed at the G1, G1/S and S phase of derived endoderm. We compared the transcriptome between these data sets and identified genes with differentiated phase expression between hESCs and hESC-derived endoderm cells.

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Activin/Nodal signalling controls divergent transcriptional networks in pluripotent and endoderm progenitors.

Project description:Activin/Nodal signalling is necessary to maintain pluripotency of human Embryonic Stem Cells (hESCs) and to induce their differentiation towards endoderm. However, the mechanisms by which Activin/Nodal signalling achieves these opposite functions remain unclear. To unravel these mechanisms, we examined the transcriptional network controlled in hESCs by Smad2 and Smad3 which represent the direct effectors of Activin/Nodal signalling. These analyses reveal that Smad2/3 participate in the control of the core transcriptional network characterising pluripotency which includes Oct-4, Nanog, FoxD3, Dppa4, Tert, Myc and UTF-1. In addition, similar experiments performed on endoderm cells confirm that a broad part of the transcriptional network directing differentiation is downstream of Smad2/3. Therefore, Activin/Nodal signalling appears to control divergent transcriptional networks in hESCs and in endoderm. Importantly, we observed an overlap between the transcriptional network downstream of Nanog and Smad2/3 in hESCs while functional studies showed that both factors cooperate to control the expression of pluripotency genes. Therefore, the effect of Activin/Nodal signalling on pluripotency and differentiation could be dictated by tissue specific Smad2/3 partners such as Nanog, explaining the mechanisms by which signalling pathways can orchestrate divergent cell fate decisions. Identification of Smad2/3 binding sites in pluripotent hESCs. 5 ChIP-Seq samples including 1 input control sample and 4 ChIP samples (two conditions x two replicates).

2011-11-11 | E-GEOD-19461 | biostudies-arrayexpress

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [targeted exome sequencing]

Project description:Human embryonic stem cells (hESC) and cancer cells rapidly divide with a short G1/S-phase causing increased replicative stress (RS). Since both in vitro cultured hESCs and most high-risk neuroblastomas have large chromosome 17q gains (17q+), we hypothesize that this may provide a "RS-resistance phenotype". We co-cultured parental cells and a derived hESC line with 17q+ under normal growth conditions and under RS. We could show a proliferative ad-vantage of hESC with 13q+17q+ over wild type by measurement of the cumulative growth and molecular analysis for chromosomal copy number analysis. To monitor effects of 17q+ on RS-resistance, cell cycle and transcriptome analysis were performed. In conclusion, we show that extra chromosomal aberrations, such as 17q+, provide proliferative advantage to hESC under RS and suggest that this phenomenon explains the high incidence of 17q+ in in vitro cultured hESC lines.

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Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [sWGS]

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Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [RNA-Seq]

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Genome Wide Profiling of p53 Response to Differentiation or DNA Damage of Human Embryonic Stem Cells

Project description:Tumor suppressor p53 promotes differentiation of human embryonic stem cells (hESCs), but an in-depth understanding of mechanism is lacking. Here, we define p53 functions in hESCs by genome wide profiling of p53 chromatin interactions and intersection with gene expression during early differentiation and in response to DNA damage. During differentiation, p53 targets and regulates a unique collection of genes, many of which encode transcription factors and developmental regulators with chromatin structure poised by OCT4 and NANOG and marked by repressive H3K27me3 in pluripotent hESCs. In contrast, genes associated with cell migration and motility are bound by p53 specifically after DNA damage. Surveillance functions of p53 in regulation of cell death and cell cycle genes are conserved during both DNA damage and differentiation. Our findings expand the registry of p53 -regulated genes in hESCs and define specific functions of p53 in opposing pluripotency, which are highly distinct from stress-induced p53 response in stem cells. Identification of p53 binding sites in hESC under three conditions : Pluripotent, DNA damaged, Differentiating

2013-10-18 | E-GEOD-39912 | biostudies-arrayexpress

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2011-05-21 | E-GEOD-29422 | biostudies-arrayexpress

Transcriptional profiling by array of human cardiac progenitors and cardiomyocytes generated from embryonic bodies, directed differentiation of hESCs with PDGFa or co-culturing hESCs with END2 cell line.

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Methylation analysis of human embryonic stem cells (hESCs), hESC-derived splanchnic mesoderm and hESC-derived mesothelium (mesenchymal form)

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