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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (ChIP-Seq)

ABSTRACT: Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (ChIP-Seq)

PROVIDER: PRJNA508527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10247800.fastq.gz	Fastqsanger.gz
	SRR10247801.fastq.gz	Fastqsanger.gz
	SRR10247802.fastq.gz	Fastqsanger.gz
	SRR10247803.fastq.gz	Fastqsanger.gz
	SRR10247804.fastq.gz	Fastqsanger.gz

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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (Bisulfite-Seq)

Project description:The genomes of mammalian neurons contain uniquely high levels of non-CG DNA methylation that can be bound by the Rett syndrome protein, MeCP2, to regulate gene expression. How patterns of non-CG methylation at genes are established and the mechanism by which this methylation works with MeCP2 to control gene expression is unclear. Here we find that genes repressed by MeCP2 are found within regions of high non-CG methylation that are defined by domains of chromatin folding. Rather than working directly at transcriptional start sites to regulate these genes, MeCP2 represses enhancer elements that are enriched for methylated cytosines occurring in the CA or CG context. Enhancers repressed by MeCP2 are found within genes that are upregulated upon loss of the protein, providing a regulatory logic for how disruption of MeCP2 can lead to wide-spread changes in gene expression. Hence, we have found that DNA topology can shape non-CG DNA methylation across the genome to dictate MeCP2-mediated enhancer regulation in the brain.

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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (RNA-Seq)

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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (ChIP-Seq)

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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression

Project description:Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression

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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (RNA-Seq)

Project description:Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (RNA-Seq)

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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (Bisulfite-Seq)

Project description:Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression (Bisulfite-Seq)

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Chromosome topology shapes neuronal non-CG DNA methylation to influence MeCP2-mediated enhancer repression

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-11-26 | GSE123373 | GEO

Transcription in Mecp2 null and Cfp1 null cells

Project description:The dinucleotide sequence 5'CG acts as a signalling module that can influence the epigenome and modulate chromosome function. CG exists in three chemically distinct forms that differ due to the modification status of the cytosine base: unmethylated, methylated or hydroxymethylated. The Cfp1 protein binds to unmethylated CG clusters in vivo and is required for the coincident trimethylation of lysine 4 in histone H3 by the Setd1 complex. On the other hand, the methyl-CG binding protein MeCP2 can direct deacetylation of histones. These findings align with evidence that nonmethylated CpG islands mark promoters, whereas CG methylation leads to gene silencing. Interfering with Cfp1 or Mecp2 function will therefore impact chromatin structure, possibly resulting in alteration of transcription. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ Abstract: This project aims to assess effects of Cfp1- and Mecp2-deficiency on transcription using RNA-seq of nascent RNA. This involves in vitro run-on transcription with isolated nuclei using BrU as a substrate to permit purification of nascent RNA. This technique shows where active polymerases are loaded on chromatin, unlike conventional RNA-seq, which only detects stable cytoplasmic RNAs.

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Swapping the DNA binding domain of MeCP2 with that of MBD2 to abolish binding to non-CG methlyation results in RTT-like phenotypes in mice [RNA-seq]

Project description:Mutations in the MECP2 gene cause the profound neurological disorder Rett syndrome. MeCP2 protein is an epigenetic reader that recruits the NCOR1/2 corepressor complexes to methylated cytosine in its canonical CG setting, but also to methylated CA motifs, which are abundant in neurons but rare in other cell types. In this study we set out to test the biological significance of this non-canonical mode of DNA binding. To achieve this, we replaced the endogenous MeCP2 DNA binding domain with that of MBD2, which only binds mCG. Knock-in mice expressing the hybrid “MM2” protein created by this domain-swap displayed severe Rett syndrome-like phenotypes. This indicates that binding to mCA, specifically the mCAC trinucleotide, is critical for normal brain function and it offers a plausible explanation for the delayed onset of Rett syndrome, due to the coincident late accumulation of mCAC and its cognate interpreter, MeCP2. We show that the small subset of genes aberrantly expressed in both Mecp2-null and MM2 mice is strikingly enriched for genes implicated in neurological disorders, highlighting targets with potential relevance to the Rett syndrome phenotype

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