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A central role for TFIID in the pluripotent transcription circuitry

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

ORGANISM(S): Mus musculus

SUBMITTER: Marian Groot Koerkamp

PROVIDER: E-GEOD-33646 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A central role for TFIID in the pluripotent transcription circuitry.

Pijnappel W W M Pim WW Esch Daniel D Baltissen Marijke P A MP Wu Guangming G Mischerikow Nikolai N Bergsma Atze J AJ van der Wal Erik E Han Dong Wook DW Bruch Hermann vom Hv Moritz Sören S Lijnzaad Phillip P Altelaar A F Maarten AF Sameith Katrin K Zaehres Holm H Heck Albert J R AJ Holstege Frank C P FC Schöler Hans R HR Timmers H T Marc HT

Nature 20130317 7442

Embryonic stem (ES) cells are pluripotent and characterized by open chromatin and high transcription levels, achieved through auto-regulatory and feed-forward transcription factor loops. ES-cell identity is maintained by a core of factors including Oct4 (also known as Pou5f1), Sox2, Klf4, c-Myc (OSKM) and Nanog, and forced expression of the OSKM factors can reprogram somatic cells into induced pluripotent stem cells (iPSCs) resembling ES cells. These gene-specific factors for RNA-polymerase-II-m ...[more]

PMID: 23503660

Similar Datasets

A central role for TFIID in the pluripotent transcription circuitry [PP002]

Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states. Two Taf5 knockdown cell lines and two control knockdown lines were each grown in duplicate and analysed on microarray against a pool of RNA from the parental ES-cells

2013-03-21 | E-GEOD-33644 | biostudies-arrayexpress

A central role for TFIID in the pluripotent transcription circuitry [PP003]

Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states. Three iPS lines, iPS#1, iPS#4, and iPS#5 were used in duplicate for microarray analysis against a pool of RNA from ES-cells.

2013-03-21 | E-GEOD-33645 | biostudies-arrayexpress

EH001: Lmx1a is an activator of Rgs4 and Gbr10 and is responsible for the correct specification of rostral and medial mdDA neurons

Project description:The LIM homeodomain transcription factor Lmx1a is a very potential inducer of stem cells towards dopaminergic neurons. Despite several studies on the function of this gene, the exact in vivo role of Lmx1a in mesodiencephalic dopamine (mdDA) neuronal specification is still not understood. To analyze the genes functioning downstream of Lmx1a, we performed expression microarray analysis of LMX1A overexpressing MN9D dopaminergic cells. Several interesting regulated genes were identified, based on their regulation in other, previously generated expression arrays, and their expression pattern in the developing mdDA neuronal field. Post analysis through in vivo expression analysis in Lmx1a mouse mutant (drJ/drJ) embryos demonstrated a clear decrease in expression of the genes Grb10 and Rgs4, in and adjacent to the rostral and dorsal mdDA neuronal field and within the Lmx1a expression domain. Interestingly, the DA marker Vmat2 was significantly up-regulated as a consequence of increased LMX1A dose, and subsequent analysis on Lmx1a mutant E14.5 and adult tissue revealed a significant decrease in Vmat2 expression in mdDA neurons. Taken together, microarray analysis of an LMX1A overexpression cell system resulted in the identification of novel downstream targets of Lmx1A in mdDA neurons: Grb10, Rgs4 and Vmat2. RNA was isolated from MN9D cells. Each experimental sample consisted of a RNA pool derived from 3 separate 10-cm dishes containing Lmx1a overexpressing MN9D cells (transfected with pcDNA3.1(-)-Lmx1a). microarray analysis was performed in triplicate, each experimental sample was hybridized to the same reference pool of RNA derived from 9 10-cm dishes containing control MN9D cells (transfected with empty pcDNA3.1(-)). On each of three microarray samples, dye swap was performed to correct for dye effects.

2013-01-08 | E-GEOD-39174 | biostudies-arrayexpress

CP003: Modulation of glutamine metabolism by the PI3K-PKB/c-akt-FOXO network regulates autophagy

Project description:The PI3K-PKB/c-akt-FOXO signalling network provides a major intracellular hub for regulation of cell proliferation, survival and stress resistance1. Here we report a novel function for FOXO transcription factors in regulating autophagy through modulation of intracellular glutamine levels. To identify novel transcriptional targets of this module we performed an unbiased microarray analysis after conditional activation of the key components PI3K, PKB, FOXO3 and FOXO4. Utilising this global pathway approach we identified glutamine synthetase (GS) as being transcriptionally regulated by PI3K-PKB-FOXO signalling. FOXO-mediated increase in GS expression specifically induced glutamine production independently of cell type, and this was evolutionary conserved. FOXO activation resulted in mTOR inhibition by preventing the translocation of mTOR to lysosomal membranes, which was dependent on GS activity. Increased GS activity resulted in increased autophagosome turnover as measured by LC3 lipidation, p62 degradation, and confocal imaging of LC3, p62, WIPI-1, ULK2 and Atg12. Inhibition of FOXO3-mediated autophagy resulted in increased apoptosis, suggesting that the induction of autophagy by FOXO3-mediated upregulation of GS is important for cellular survival. These findings reveal a novel signalling network that can directly modulate autophagy through regulation of glutamine metabolism. conditional activation of foxo3 and foxo4 were followed in a timeseries. Each timepoint consists of 4 independent replicates, labeled with either cy3 or cy5 and put on array against time0 as reference.

2012-07-21 | E-GEOD-35703 | biostudies-arrayexpress

WB001A: Genome-wide analysis reveals NRP1 as a critical HIF1-E2F7 target gene in the regulation of motor neuron guidance in vivo

Project description:In this study, we explored the existence of a transcriptional network co-regulated by E2F7 and HIF1Î±, as we show that expression of E2F7, like HIF1Î±, is induced in hypoxia, and because of the previously reported ability of E2F7 to interact with HIF1Î±. Our genome-wide analysis uncovers a transcriptional network that is directly controlled by HIF1Î± and E2F7, and demonstrates both stimulatory and repressive functions of the HIF1Î± -E2F7 complex. Among this network we reveal Neuropilin 1 (NRP1) as a HIF1Î±-E2F7 repressed gene. By performing in vitro and in vivo reporter assays we demonstrate that the HIF1Î±-E2F7 mediated NRP1 repression depends on a 41 base pairs 'E2F-binding site hub', providing a molecular mechanism for a previously unanticipated role for HIF1Î± in transcriptional repression. To explore the biological significance of this regulation we performed in situ hybridizations and observed enhanced nrp1a expression in spinal motorneurons (MN) of zebrafish embryos, upon morpholino-inhibition of e2f7/8 or hif1Î±. Consistent with the chemo-repellent role of nrp1a, morpholino-inhibition of e2f7/8 or hif1Î± caused MN truncations, which was rescued in TALEN-induced nrp1a(hu10012) mutants, and phenocopied in e2f7/8 mutant zebrafish. Therefore, we conclude that repression of NRP1 by the HIF1Î±-E2F7 complex regulates MN axon guidance in vivo. The following samples were analyzed by microarrays: RNA isolated from HeLa cells transfected with either control (scr), E2F7, HIF1a, E2F7 and E2F8, or E2F7 and HIF1a siRNAs. Cells were harvested 48h after transfection, and were grown the last 16h in hypoxia. RNA isolated from scr-transfected, normoxic HeLa cells was used as common reference RNA. Within each group of two biological replicates, sample versus common reference hybridisations were performed in balanced dye-swap. Microarrays used were human whole genome gene expression microarrays V1 (Agilent, Belgium).

2016-01-04 | E-GEOD-66750 | biostudies-arrayexpress

RNAi profiling by array of human HEp-2 cells with siRNA-mediated depletion of RNase MRP protein components

Project description:To identify mRNA substrates for the human RNase MRP complex, we examined the effects of siRNA-mediated depletion of RNase MRP (and RNase P) on the transcriptome of HEp-2 cells. The expression of two RNase MRP protein components, hPop1 and Rpp40, was knocked-down and after 48 hours mRNA was isolated from these cells as well as from cells transfected with an siRNA targeting the GFP mRNA (siEGFP), which was used as a control. The expression levels of mRNAs were analyzed on a genome-wide scale using 21K microarrays.

2011-04-01 | E-TABM-981 | biostudies-arrayexpress

Transcriptional profiling of Caenorhabditis elegans whole-organism extract and subsequent co-immune precipitation of mRNA with the poly-A binding protein FLAG::PAB-1 specifically expressed in body wall muscle cells.

Project description:Tissue specific microarray data is obtained by generating a whole-organism extract and subsequent co-immune precipitation of mRNA with the poly-A binding protein FLAG::PAB-1 specifically expressed in body wall muscle cells (Roy et al. 2002). Different lines were compared: SV911 (control), SV912 (CYE-1/CDK-2AF), and SV985 (CYD-1/CDK-4). As reference total RNA was used.

2011-11-25 | E-TABM-886 | biostudies-arrayexpress

siRNA profiling of human MCF7 cells with elimination of either TFAP2C or TFAP2A reveals TFAP2C regulates multiple pathways of estrogen signaling

Project description:We were interested in determining what genes might be controlled by TFAP2C and/or TFAP2A, either directly or indirectly through regulation of ER-alpha and potentially other signaling pathways. We performed an microarray analysis in MCF7 cells with elimination of either TFAP2C or TFAP2A. The patterns of gene expression with alteration of TFAP2 activity were compared to changes in expression induced by estrogen exposure. Knock-down of TFAP2C in the presence of estrogen altered the pattern of several known ERalpha-regulated genes and a number of genes outside the estrogen-regulated pathways. Experiment Overall Design: 6 samples were analyzed. Experiment Overall Design: 1. MCF7 cells treated with TFAP2C siRNA, without the presence of estrogen. Experiment Overall Design: 2.MCF7 cells treated with TFAP2C siRNA, with the presence of estrogen. Experiment Overall Design: 3.MCF7 cells treated with TFAP2A siRNA, without the presence of estrogen. Experiment Overall Design: 4.MCF7 cells treated with TFAP2A siRNA, with the presence of estrogen. Experiment Overall Design: 5.MCF7 cells with no siRNA treatment, without the presence of estrogen. Experiment Overall Design: 6.MCF7 cells with no siRNA treatment, with the presence of estrogen.

2008-06-16 | E-GEOD-8640 | biostudies-arrayexpress

docetaxel response prediction MEEBO

Project description:Using gene expression profiling of mammary tumors generated in a mouse model for BRCA1-associated breast cancer we have searched for markers that correlate with response to the anti-cancer drugs docetaxel or cisplatin. To validate the results, the analysis was done on 2 different platforms (39K Mouse Exonic Evidence Based Oligonucleotide (MEEBO), and 45K Illumina Sentrix mouse V6 single-channel bead arrays). Moreover, we analyzed mouse mammary tumors that had acquired docetaxel resistance on the MEEBO platform.

2011-10-26 | E-MTAB-415 | biostudies-arrayexpress

Transcription profiling of human CD34+ derived neutrophil progenitors from umbilical cord blood, in response to Mek1 activation

Project description:analysis of differential gene expression in CD34+ derived neutrophil progenitors from umbilical cord blood, in response to Mek1 activation

2009-08-14 | E-TABM-754 | biostudies-arrayexpress

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