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E-MEXP-701

ABSTRACT: Transcription profiling by array of mouse primary dermal fibroblasts after treatment with 5-aza-2'-deoxycytidine

OTHER RELATED OMICS DATASETS IN: PRJNA96743PRJNA96745

PROVIDER: E-MEXP-701 | ExpressionAtlas | 2015-10-22

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MEXP-701-analysis-methods.tsv	Tabular
	E-MEXP-701-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-701-configuration.xml	Xml
	E-MEXP-701-percentile-ranks.tsv	Tabular
	E-MEXP-701.condensed-sdrf.tsv	Tabular

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Transcription profiling of primary mouse dermal fibroblasts, chondrocytes and osteoblasts treated with 5-aza-2?-deoxycytidine for 96/72h to identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation

Project description:DNA methylation can contribute to the stable transcriptional silencing of mammalian genes. Oftentimes, these genes are important developmental regulators, and their silencing in cell types where they are not supposed to be active is important for the phenotypic stability of the cells. To identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation, mouse dermal fibroblasts were demethylated with 5-aza-2-deoxycytidine, and changes in gene expression monitored by microarray analysis. Three biological replicates for both control and 5-aza-2'-deoxycytidine treatment were derived. Cells were primary mouse dermal fibroblasts, primary mouse chondrocytes, and primary mouse osteoblasts derived separately for each biological replicate. Treated cells were exposed to 5uM 5-aza-2'-deoxycytidine for 96 hours with recovery in normal medium for 24 hours. Control cells were untreated.

2007-11-23 | E-GEOD-4768 | biostudies-arrayexpress

Transcription profiling of mouse primary dermal fibroblasts treated with the de-methylating agent 5-aza-2?-deoxycytidine vs untreated to investigate methylation related changes in gene expression

Project description:DNA methylation can contribute to the stable transcriptional silencing of mammalian genes. Oftentimes, these genes are important developmental regulators, and their silencing in cell types where they are not supposed to be active is important for the phenotypic stability of the cells. To identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation, mouse dermal fibroblasts were demethylated with 5-aza-2-deoxycytidine, and changes in gene expression monitored by microarray analysis. Three biological replicates for both control and 5-aza-2'-deoxycytidine treatment were derived. Cells were primary mouse dermal fibroblasts derived by explant procedure separately for each biological replicate. Treated cells were exposed to 5uM 5-aza-2'-deoxycytidine for 96 hours with recovery in normal medium for 24 hours. Control cells were untreated.

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Transcription profiling of mouse primary dermal fibroblasts treated with DNA demethylating agent 5-aza-2-deoxycytidine

Project description:Mouse primary dermal fibroblasts were treated with DNA demethylating agent 5-aza-2'-deoxycytidine. The exposure was 5um 5A2dC for 96 hours followed by recovery in normal medium for 24 hours. Three biological replicates were created for both the control and treated populations. Each biological replicate represents a separate derivation of dermal fibroblasts from genetically identical mouse pups aged 0-3 days. Cells reached passage 4 before initiating drug exposure.

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CG methylated microarrays identify novel methylated sequence bound by the CEBPB|ATF4 heterodimer that are active in vivo

Project description:To evaluate the effect of CG methylation on DNA binding of sequence-specific B-ZIP transcription factors (TFs) in a high-throughput manner, we enzymatically methylated the cytosine in the CG dinucleotide on protein binding microarrays. Using this novel technology, we show that CG methylation enhanced binding for CEBPA and CEBPB and inhibited binding for CREB, ATF4, JUN, JUND, CEBPD and CEBPG. The CEBPB|ATF4 heterodimer bound a novel motif CGAT|GCAA 10-fold better when methylated. EMSA confirmed these results. CEBPB ChIP-seq data using primary female mouse dermal fibroblasts with 50X methylome coverage for each strand indicate that the methylated sequences well-bound on the arrays are also bound in vivo. CEBPB bound 39% of the methylated canonical 10-mers ATTGC|GCAAT in the mouse genome. After ATF4 protein induction by thapsigargin which results in ER stress, CEBPB binds methylated CGAT|GCAA in vivo, recapitulating what was observed on the arrays. mRNA-seq of primary female mouse dermal fibroblasts with and without thapsigargin identified differentially expressed genes. Genes that are commonly bound by CEBPB and ATF4 to TGAT|GCAA (the best-bound 8-mer in the array) at the promoters were highly expressed and up-regulated or remained unchanged in the thapsigargin treated primary female mouse dermal fibroblasts. RNA-Seq: Examination of whole genome transcriptome profiles (RNA-seq) of primary mouse dermal fibroblasts with and without Thapsigargin treatment ChIP-Seq: Examination of transcription factor binding in dermal fibroblasts with and without Thapsigargin teratment BS-Seq: Determination of whole genome DNA methylation profiles (BS-seq) of primary mouse dermal fibroblasts

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Mus musculus

Project description:Gene expression changes following demethylation by 5-aza-2'-deoxycytidine in primary mouse dermal fibroblasts

| PRJNA96745 | ENA