Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Functional DNA methylation is accompanied by chromatin accessibility [gene expression]

ABSTRACT: Analysis of nucleosome positioning and chromatin state by using CpG methyltransferase M.SssI to methylate nuclei. Unmethylated regions that gain methylation (low to high beta value) are known to be accessible and nucleosome depleted. Method used to study changes after epigenetic drug treatments identified that majority of demethylation events are not accompanied by chromatin accessibility changes. RNA harvested from cells post epigenetic drug treatment, with 5-Aza-CdR or SAHA

ORGANISM(S): Homo sapiens

SUBMITTER: Kurinji Pandiyan

PROVIDER: E-GEOD-43852 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Functional DNA demethylation is accompanied by chromatin accessibility.

Pandiyan Kurinji K You Jueng Soo JS Yang Xiaojing X Dai Chao C Zhou Xianghong J XJ Baylin Stephen B SB Jones Peter A PA Liang Gangning G

Nucleic acids research 20130213 7

DNA methylation inhibitors such as 5-aza-2'-deoxycytidine (5-Aza-CdR) are currently used for the treatment of myelodysplastic syndrome. Although global DNA demethylation has been observed after treatment, it is unclear to what extent demethylation induces changes in nucleosome occupancy, a key determinant of gene expression. We use the colorectal cancer cell line HCT116 as a model to address this question and determine that <2% of regions demethylated by 5-Aza-CdR treatment assume an open config ...[more]

PMID: 23408854

Similar Datasets

Functional DNA methylation is accompanied by chromatin accessibility [methylation]

Project description:Analysis of nucleosome positioning and chromatin state by using CpG methyltransferase M.SssI to methylate nuclei. Unmethylated regions that gain methylation (low to high beta value) are known to be accessible and nucleosome depleted. Method used to study changes after epigenetic drug treatments identified that majority of demethylation events are not accompanied by chromatin accessibility changes. Intact nuclei are harvested from cells and treated with M.SssI. DNA is then extracted, bisulfite converted and run on an Infinium methylation array, along with a no-enzyme control. Background subtracted beta values (listed below) are used to determine regions that have gained methylation on enzyme treatment compared to the control - and these are used to infer chromatin state

2013-03-08 | E-GEOD-43851 | biostudies-arrayexpress

Functional DNA methylation is accompanied by chromatin accessibility [methylation]

2013-03-08 | GSE43851 | GEO

Functional DNA methylation is accompanied by chromatin accessibility [gene expression]

2013-03-08 | GSE43852 | GEO

AcceSssIble: an array-based assay for the study of chromatin accessibility and DNA methylation using the CpG methyltransferase SssI

Project description:Analysis of nucleosome positioning and chromatin state by using CpG methyltransferase M.SssI to methylate nuclei. Unmethylated regions that gain methylation (low to high beta value) are known to be accessible and nucleosome depleted. Intact nuclei are harvested from cells and treated with M.SssI. DNA is then extracted, bisulfite converted and run on an Infinium methylation array, along with a no-enzyme control. Background subtracted beta values (listed below) are used to determine regions that have gained methylation on enzyme treatment compared to the control - and these are used to infer chromatin state

2013-03-08 | E-GEOD-36580 | biostudies-arrayexpress

AcceSssIble: an array-based assay for the study of chromatin accessibility and DNA methylation using the CpG methyltransferase SssI

2013-03-08 | GSE36580 | GEO

HEK 293T cells HELP-tagging cytosine methylation data treated with 5-aza-2-deoxycytidine

Project description:DNA methylation can be abnormally regulated in human disease and associated with effects on gene transcription that appear to be causally related to pathogenesis. The potential to use pharmacological agents that reverse this dysregulation is therefore an attractive possibility. To test how 5-aza-2M-bM-^@M-^Y-deoxycytidine (5-aza-CdR) influences the genome therapeutically, we exposed non-malignant cells in culture to the agent and used genome-wide assays to assess the cellular response. We found that cells allowed to recover from 5-aza-CdR treatment only partially recover DNA methylation levels, retaining an epigenetic M-bM-^@M-^\imprintM-bM-^@M-^] of drug exposure. We show very limited transcriptional responses to demethylation of not only protein-coding genes but also loci encoding non-coding RNAs, with a limited proportion of the induced genes acquiring new promoter activation within gene bodies. The data revealed an uncoupling of DNA methylation effects at promoters, with demethylation mostly unaccompanied by transcriptional changes. The limited panel of genes induced by 5-aza-CdR resembles those activated in other human cell types exposed to the drug, and represents loci targeted for Polycomb-mediated silencing in stem cells, suggesting a model for the therapeutic effects of the drug. Our results do not support the hypothesis of DNA methylation having a predominant role to regulate transcriptional noise in the genome, and indicate that DNA methylation acts only as part of a larger complex system of transcriptional regulation. The targeting of 5-aza-CdR effects with its clastogenic consequences to euchromatin raises concerns that the use of 5-aza-CdR has innate tumorigenic consequences, requiring its cautious use in diseases involving epigenetic dysregulation. Cytosine methylation profile of 4 different samples of HEK 293T treated with 5-aza-CdR

2015-02-13 | E-GEOD-62592 | biostudies-arrayexpress

HEK 293T cells RNA-seq data treated with 5-aza-2-deoxycytidine

Project description:DNA methylation can be abnormally regulated in human disease and associated with effects on gene transcription that appear to be causally related to pathogenesis. The potential to use pharmacological agents that reverse this dysregulation is therefore an attractive possibility. To test how 5-aza-2M-bM-^@M-^Y-deoxycytidine (5-aza-CdR) influences the genome therapeutically, we exposed non-malignant cells in culture to the agent and used genome-wide assays to assess the cellular response. We found that cells allowed to recover from 5-aza-CdR treatment only partially recover DNA methylation levels, retaining an epigenetic M-bM-^@M-^\imprintM-bM-^@M-^] of drug exposure. We show very limited transcriptional responses to demethylation of not only protein-coding genes but also loci encoding non-coding RNAs, with a limited proportion of the induced genes acquiring new promoter activation within gene bodies. The data revealed an uncoupling of DNA methylation effects at promoters, with demethylation mostly unaccompanied by transcriptional changes. The limited panel of genes induced by 5-aza-CdR resembles those activated in other human cell types exposed to the drug, and represents loci targeted for Polycomb-mediated silencing in stem cells, suggesting a model for the therapeutic effects of the drug. Our results do not support the hypothesis of DNA methylation having a predominant role to regulate transcriptional noise in the genome, and indicate that DNA methylation acts only as part of a larger complex system of transcriptional regulation. The targeting of 5-aza-CdR effects with its clastogenic consequences to euchromatin raises concerns that the use of 5-aza-CdR has innate tumorigenic consequences, requiring its cautious use in diseases involving epigenetic dysregulation. mRNA profile of 5 different samples of HEK 293T cells treated with 5-aza-CdR

2015-02-13 | E-GEOD-62591 | biostudies-arrayexpress

Genome-wide maps of RNAPII Ser5(P) in HEK 293T cells after treatment with 5-aza-CdR

Project description:DNA methylation can be abnormally regulated in human disease and associated with effects on gene transcription that appear to be causally related to pathogenesis. The potential to use pharmacological agents that reverse this dysregulation is therefore an attractive possibility. To test how 5-aza-2M-bM-^@M-^Y-deoxycytidine (5-aza-CdR) influences the genome therapeutically, we exposed non-malignant cells in culture to the agent and used genome-wide assays to assess the cellular response. We found that cells allowed to recover from 5-aza-CdR treatment only partially recover DNA methylation levels, retaining an epigenetic M-bM-^@M-^\imprintM-bM-^@M-^] of drug exposure. We show very limited transcriptional responses to demethylation of not only protein-coding genes but also loci encoding non-coding RNAs, with a limited proportion of the induced genes acquiring new promoter activation within gene bodies. The data revealed an uncoupling of DNA methylation effects at promoters, with demethylation mostly unaccompanied by transcriptional changes. The limited panel of genes induced by 5-aza-CdR resembles those activated in other human cell types exposed to the drug, and represents loci targeted for Polycomb-mediated silencing in stem cells, suggesting a model for the therapeutic effects of the drug. Our results do not support the hypothesis of DNA methylation having a predominant role to regulate transcriptional noise in the genome, and indicate that DNA methylation acts only as part of a larger complex system of transcriptional regulation. The targeting of 5-aza-CdR effects with its clastogenic consequences to euchromatin raises concerns that the use of 5-aza-CdR has innate tumorigenic consequences, requiring its cautious use in diseases involving epigenetic dysregulation. Examination of RNAPII Ser5(P) localization by ChIP-seq in HEK 293T cell after treatment with 5-aza-CdR.

2015-02-13 | E-GEOD-62695 | biostudies-arrayexpress

RNA sequencing revealed novel actors of the acquisition of drug resistance in Candida albicans

Project description:Drug susceptible clinical isolates of Candida albicans frequently become highly tolerant to drugs during chemotherapy, with dreadful consequences on patient health. We used RNA sequencing (RNA-seq) to analyze the transcriptomes of a CDR (Candida Drug Resistance) strain and its isogenic drug sensitive counterpart. RNA-seq unveiled differential expression of 228 genes including a) genes previously identified as involved in CDR, b) genes not previously associated to the CDR phenotype, and c) novel transcripts whose function as a gene is uncharacterized. In particular, we show for the first time that CDR acquisition is correlated with an overexpression of the transcription factor encoding gene CZF1. CZF1 null mutants were sensitive to many drugs, independently of known multidrug resistance mechanisms. We show that CZF1 acts as a repressor of M-NM-2-glucan synthesis, thus negatively regulating cell wall integrity. Finally, our RNA-seq data allowed us to identify a new transcribed region, upstream of the TAC1 gene, which encodes the major CDR transcriptional regulator. Our results open new perspectives to the role of Czf1 and to our understanding of the transcriptional and post-transcriptional mechanisms that lead to the acquisition of drug resistance in C. albicans, with potential future improvements of therapeutic strategies. RNA sequencing was performed on 2 Candida albicans strains (Gu4 and Gu5). For each strain, we sequenced 2 biological replicates.

2012-09-04 | E-GEOD-38298 | biostudies-arrayexpress

Transcription profiling of human gastric cancer cells after treatment with 5-aza-2-deoxycytidine and 4-phenylbutyric acid

Project description:Gene expression profiling in human gastric cancer cells after 5-aza-2'-deoxycytidine (5-Aza-CdR) and 4-phenylbutyric acid (PBA) treatment was analyzed to investigate what genes are controlled by these chromatin modifying drug

2008-10-09 | E-MEXP-1821 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data