Dataset Information


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

ABSTRACT: 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. Overall design: Examine Mbd2 and Mbd3 occupancy (ChIP-seq) in ES cells

INSTRUMENT(S): Illumina HiSeq 2000 (Mus musculus)

SUBMITTER: Sarah J Hainer  

PROVIDER: GSE86965 | GEO | 2016-11-15



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DNA methylation directs genomic localization of Mbd2 and Mbd3 in embryonic stem cells.

Hainer Sarah J SJ   McCannell Kurtis N KN   Yu Jun J   Ee Ly-Sha LS   Zhu Lihua J LJ   Rando Oliver J OJ   Fazzio Thomas G TG  

eLife 20161116

Cytosine methylation is an epigenetic and regulatory mark that functions in part through recruitment of chromatin remodeling complexes containing methyl-CpG binding domain (MBD) proteins. Two MBD proteins, Mbd2 and Mbd3, were previously shown to bind methylated or hydroxymethylated DNA, respectively; however, both of these findings have been disputed. Here, we investigated this controversy using experimental approaches and re-analysis of published data and find no evidence for methylation-indepe  ...[more]

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