Expression data from mouse embryonic fibroblasts and pluripotent stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Takuya Yamamoto
PROVIDER: E-GEOD-45916 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:By combining deep sequencing with high-throughput quantitative RT-PCR, we reveal that somatic splicing profiles are reorganized to pluripotent splicing profiles during reprogramming from mouse embryonic fibroblasts (MEFs) to induced pluripotent stem (iPS) cells. The splicing pattern in pluripotent stem cells resembles that in testis, and the regulatory regions have specific characters in length and sequence. These results indicate that the dynamic alteration in splicing is an integral part of the molecular network involved in the reprogramming process. Sequencing data from MEF, two iPS cell lines and one ES cell line. RT-PCR data will be represented within Figures or Tables in published manuscripts.
2013-10-17 | E-GEOD-46149 | biostudies-arrayexpress
Project description:The Akita mutation (C96Y) in the insulin gene results in early onset diabetes in both humans and mice. Expression of the mutant proinsulin (C96Y) causes endoplasmic reticulum (ER) stress in pancreatic ?-cells and consequently the cell activates the unfolded protein response (UPR). Since the proinsulin is terminally misfolded however, the ER stress is irremediable and chronic activation of the UPR eventually activates apoptosis in the cell population. We used microarray gene expression arrays to analyze the IRE1-dependent activation of genes in response to misfolded proinsulin expression in an inducible mutant proinsulin (C96Y) insulinoma cell line by inhibiting the IRE1 endoribonucleas activity with a specific inhibitor, 4u8c. Insulinoma cells with doxycycline inducible C96Y-proinsulin expression were either untreated, treated with doxycycline alone or treated with dox and 4u8c. This was done with two biological replicates.
2014-07-16 | E-GEOD-58866 | biostudies-arrayexpress
Project description:Prostate cancer C4-2B cells were cultured in enzalutamide in a dose-escalation manner. After sixty passages cells were resistant to enzalutamide, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for enzalutamide resistance in C4-2B-MDVR cells. Enzalutamide resistant C4-2B-MDVR cells were selected from C4-2B cells during long time enzalutamide treatment. Genes responsible for enzalutamide resistance were identified using C4-2B vs. C4-2B-MDVR RNA extraction and hybridization on Affymetrix microarrays.
2015-04-09 | E-GEOD-64143 | biostudies-arrayexpress
Project description:Prostate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for docetaxel resistance in TaxR cells. Docetaxel resistant TaxR cells were selected from C4-2B cells during long time docetaxel treatment. Genes responsible for docetaxel resistance were identified using C4-2B vs. TaxR RNA extraction and hybridization on Affymetrix microarrays.
2013-08-01 | E-GEOD-47040 | biostudies-arrayexpress
Project description:Differentiating erythroid cells execute a unique gene expression program that insures synthesis of the appropriate proteome at each stage of maturation. Standard expression microarrays provide important insight into erythroid gene expression, but cannot detect qualitative changes in transcript structure, mediated by RNA processing, that alter structure and function of encoded proteins. We analyzed stage-specific changes in the late erythroid transcriptome via use of high resolution microarrays that detect altered expression of individual exons. Ten differentiation-associated changes in erythroblast splicing patterns were identified, including the previously known activation of protein 4.1R exon 16 splicing. Six new alternative splicing switches involving enhanced inclusion of internal cassette exons were discovered, as well as three changes in use of alternative first exons. All of these erythroid stage-specific splicing events represent activated inclusion of authentic annotated exons, suggesting they represent an active regulatory process rather than a general loss of splicing fidelity. The observation that three of the regulated transcripts encode RNA binding proteins (SNRP70, HNRPLL, MBNL2) may indicate significant changes in the RNA processing machinery of late erythroblasts. Together these results support the existence of a regulated alternative pre-mRNA splicing program that is critical for late erythroid differentiation. Keywords: Time course; Splicing-sensitive microarray For Exon array hybridizations: 3 biological replicates of day 7, 2 biological replicates of day 10, 3 biological replicates of day 14; For HJAY array hybridizations: 5 biological replicates each were analyzed from day 7 and day 14. One day 14 replicate was deemed an outlier and removed from subsequent analyses.
2010-05-16 | E-GEOD-14588 | biostudies-arrayexpress
Project description:The conserved SR-like protein Npl3 promotes the splicing of diverse pre-mRNAs. However, the RNA sequence(s) recognized by the RNA Recognition Motifs (RRM1 & RRM2) of Npl3 during the splicing reaction remain elusive. Here, we developed a split-iCRAC approach in vivo to determine the consensus sequence bound to each RRM in yeast. High-resolution NMR structures show that RRM2 recognizes a 5´-GNGG-3´ motif leading to an unusual mille-feuille topology. In addition, our data indicate a non-specific interaction of the RS domain with RNA. These structures reveal how RRM1 preferentially interacts with a CC-dinucleotide upstream of this motif, and how the inter-RRM linker and the region C-terminal to RRM2 contributes to cooperative RNA-binding. Structure-guided studies show that Npl3 genetically interacts with U2 snRNP specific factors and we provide evidence that Npl3 melts U2 snRNA stem-loop I, a prerequisite for U2/U6 duplex formation within the catalytic centre of the Bact spliceosomal complex. Our findings provide a mechanistic role for Npl3 during spliceosome active site formation.
2022-12-01 | E-MTAB-11736 | biostudies-arrayexpress
Project description:To investigate the possible range of additional RNase P substrates in vivo a strand-specific, high-density microarray was used to analyze what RNA accumulates with a mutation in the catalytic RNA subunit of nuclear RNase P in Saccharomyces cerevisiae. A wide variety of noncoding RNAs were shown to accumulate, suggesting nuclear RNase P participates in the turnover of normally unstable nuclear RNAs. In some cases, the accumulated noncoding RNAs were shown to be antisense to transcripts that commensurately decreased in abundance. Pre-mRNAs containing introns also accumulated broadly, consistent with either compromised splicing or failure to efficiently turnover pre-mRNAs that do not enter the splicing pathway. Taken together with the high complexity of the nuclear RNase P holoenzyme and its relatively non-specific capacity to bind and cleave mixed sequence RNAs, these data suggest nuclear RNase P facilitates turnover of nuclear RNAs in addition to its role in pre-tRNA biogenesis.
2011-08-29 | E-MEXP-3140 | biostudies-arrayexpress
Project description:Much remains unknown concerning the mechanism by which the splicing machinery pinpoints short exons within intronic sequences and how splicing factors are directed to their pre-mRNA targets. Part of the explanation probably lies in differences in chromatin organization between exons and introns. Proteomic, co-immunoprecipitation, and sedimentation analyses described here indicated that SF3B1, an essential splicing component of the U2 snRNP complex, is strongly associated with nucleosomes. ChIP-seq and RNA-seq analyses revealed that SF3B1 is specifically bound to nucleosomes located at exonic positions. SF3B1 binding is enriched at nucleosomes positioned over short exons flanked by long introns that are also characterized by differential GC content between exons and introns. Disruption of SF3B1 binding to such nucleosomes affected the splicing of these exons similarly to inhibition of SF3B1 expression. Our findings suggest that the association of SF3B1 with nucleosomes is functionally important for splice site recognition and that SF3B1 conveys splicing-relevant information embedded in chromatin structure. MNase-seq on Input and SF3B1 pull-down, mRNA-seq on control and SF3B1 si-RNA treated cells as well as on TSA (Trichostatin A) treated and untreated cells.
2015-04-22 | E-GEOD-65644 | biostudies-arrayexpress
Project description:We generated a global analysis of Rbfox2 splicing regulation combined with a highly specific, single nucleotide-resolution Rbfox2 RNA binding map. We found that Rbfox2 regulates the splicing and expression of many previously unknown targets, and particularly a number of RNA binding proteins (RBPs), by modulating alternative splicing coupled-NMD. Based on our observations of RBP-Rbfox2 co-regulation with a polarity predicted by Rbfox2 binding, we propose a model whereby Rbfox2 tunes autoregulatory splicing events to control RBP expression levels and in turn alter their respective splicing networks. iCLIP for epitope-tagged Rbfox2 and control untagged Rbfox2; RNAseq of control and Rbfox2 knockdown in mouse embryonic stem cells
2014-03-17 | E-GEOD-54794 | biostudies-arrayexpress
Project description:Long intervening noncoding RNAs (lincRNAs) are prevalent genes with poorly understood functions. Here we discover a pathway of lincRNA-regulated proteolysis. The enhancer-like lincRNA HOTTIP extends the half-life of its binding protein WDR5, a subunit of the MLL H3K4 methylase complex, resulting in increased chromatin occupancy and gene activation. LincRNA-mediated stabilization requires direct RNA-protein interaction in a long RNA context, and blocks turnover at a step after target protein poly-ubiquitination. We elucidate the lincRNA binding interface on WDR5. A WDR5 mutant that selectively abrogates lincRNA binding becomes unstable, and is defective in gene activation, maintenance of histone H3 lysine 4 trimethylation, and embryonic stem cell self renewal. The ability to modulate protein turnover may allow lincRNAs to control the lifespan of molecular interactions at chromatin and elsewhere, broadening their scope in epigenetics and cell fate control. Gene expression analysis: To establish a differentiation signature for mouse V6.5 ES cells infected with anti mouse WDR5 shRNA, rescued with doxycycline inducible WDR5 WT or WDR5 F266A, total RNA was isolated in biologic duplicate from cells in different conditions and hybridized to Affymetrix Mouse 430 2.0 arrays.
2013-02-18 | E-GEOD-36513 | biostudies-arrayexpress