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Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (2)

ABSTRACT: DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE63234 | GEO | 2015/06/17

SECONDARY ACCESSION(S): PRJNA267067

REPOSITORIES: GEO

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Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (3)

Project description:DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. MBD2 ChIP and input, Methylated DNA precipitation and input, in HMEC-hTERT and HMLER cell lines

2015-06-17 | E-GEOD-63235 | biostudies-arrayexpress

Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (1)

2015-06-17 | GSE63233 | GEO

Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (3)

2015-06-17 | GSE63235 | GEO

Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (1)

Project description:DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. Methylated DNA precipitation (MeDP) and Endogenous MBD2 Chromatin Immunoprecipitation (MBD2 ChIP) followed by hight-througput sequencing in HMEC-hTERT and HMLER cells.

2015-06-17 | E-GEOD-63233 | biostudies-arrayexpress

Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (2)

Project description:DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. RNAseq of untreated HMEC-hTERT cells, siCtrl, siMBD2 or DAC treated HMLER cells, siCtrl or siMBD2 treated HME-ZEB1-RAS and HME-shP53-RAS cells, in duplicates.

2015-06-17 | E-GEOD-63234 | biostudies-arrayexpress

Methylation profiles of MCF-10A cells infected with MBD2 lentivirus

2013-06-13 | GSE47857 | GEO

Methylation profiles of MCF-10A cells infected with MBD2 lentivirus

Project description:Methylated DNA binding protein 2 (MBD2) has been shown to bind specific methylated promoters and suppress transcription. Here we systematically investigate MBD2 suppression by overexpressing MBD2 in MCF-10A cells and generating genome-wide promoter methylation profiles in order to identify methylation changes likely to affect gene expression levels. MCF-10A cells were infected with MBD2 lentivirus in order to increase MBD2 expression. DNA was extracted from both infected and non-infected cells and enriched for methylated DNA through the method of methylated DNA immunoprecipitation (MeDIP). Enriched and total DNA was hybridized in different channels to 244K custom microarrays (Agilent Technologies) that contained probes covering at 100bp-spacing all transcription start sites from -800bp to 200bp (human, Ensembl v44) and all microRNAs in miRBase from 250bp before to 250bp after the microRNA. Three technical replicates were hybridized for infected and non-infected cells.

2013-06-13 | E-GEOD-47857 | biostudies-arrayexpress

MBD2 couples DNA methylation to Transposable Elements silencing during male gametogenesis

Project description:DNA methylation is an essential component of transposable element (TE) silencing, yet the mechanism by which methylation causes transcriptional repression remains poorly understood. Here we study the Arabidopsis thaliana Methyl-CpG Binding Domain (MBD) proteins MBD1, MBD2, and MBD4, and show that MBD2 acts as a transposable element (TE) repressor during male gametogenesis. MBD2 bound chromatin regions containing high levels of CG methylation, and MBD2 was capable of silencing the FWA gene when tethered to its promoter. MBD2 loss caused TE activation in the vegetative cell (VC) of mature pollen without affecting DNA methylation levels, demonstrating that MBD2-mediated silencing acts strictly downstream of DNA methylation. Loss of silencing in mbd2 became more significant in the mbd5 mbd6 or adcp1 mutant backgrounds, as well as in plants with chemically induced genome-wide DNA demethylation, suggesting that MBD2 acts redundantly with other silencing pathways to safeguard TEs from activation. Overall, our study identifies MBD2 as a novel methyl reader that acts downstream of DNA methylation to silence TEs during male gametogenesis.

2024-01-12 | GSE236290 | GEO

DNA Methylation in IMR90 cells

Project description:DNA methylation was measured by MBD2 enrichment of DNA fragments in IMR90. A statistical model was developed to estimate absolute methylation levels, and compared to whole genome bisulfite sequencing results (Lister, R. et al. (2009) Human DNA methylomes at base resolution show widespread epigenomic differences. Nature) Two techincal replicates of MBD2 methylated DNA enrichment in IMR90 cells.

2012-11-30 | E-GEOD-38679 | biostudies-arrayexpress

DNA methylation is required for chromatin binding by Mbd2 and Mbd3 in ES cells (ChIP-Seq, meDIP-seq and hmDIP-seq)

Project description:Cytosine methylation on DNA is an important epigenetic and regulatory mark. Chromatin remodeling complexes containing methyl-CpG binding domain (MBD) proteins modulate chromatin structure and transcription at methylated loci. Two MBD proteins, Mbd2 and Mbd3, are mutually exclusive members of the NuRD chromatin remodeling complex, and have been shown to bind methylated or hydroxymethylated DNA, respectively. However, a recent study called both results into question, showing that chromatin binding by these proteins is partially (Mbd2) or completely (Mbd3) independent of DNA methylation/hydroxymethylation. Here we re-analyze these data and observe discrepancies with both conclusions. Furthermore, we describe multiple new datasets that demonstrate the dependence of endogenous Mbd2 and Mbd3 on DNA methylation. Interestingly, we find that Mbd2 and Mbd3 are also dependent on one another for binding, likely due to the fact that both are required for normal levels of DNA methylation/hydroxymethylation. These findings describe a regulatory loop controlling the DNA methylation machinery and its readers.

2016-11-15 | GSE79770 | GEO

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