Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE138613 | GEO | 2019/11/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

2019-11-26 | GSE123372 | GEO

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

2019-11-26 | GSE123371 | GEO

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

| PRJNA508525 | ENA

Non-CG methylation patterns shape the epigenetic landscape in Arabidopsis

Project description:DNA methylation occurs in both CG and non-CG sequence contexts. Non-CG methylation is abundant in plants, and is mediated by CHROMOMETHYLASE (CMT) and DOMAINS REARRANGED METHYLTRANSFERASE (DRM) proteins; however its roles remain poorly understood. Here we characterize the roles of non-CG methylation in Arabidopsis thaliana. We show that a poorly characterized methyltransferase, CMT2, is a functional methyltransferase in vitro and in vivo. CMT2 specifically binds histone H3 lysine 9 (H3K9) dimethylation and methylates non-CG cytosines at sites that are also regulated by H3K9 dimethylation. By generating different combinations of non-CG methylation mutants, we reveal the contributions and redundancies between each methyltransferase in DNA methylation patterning and in regulating transposable elements (TEs) and protein-coding genes. We also demonstrate extensive dependencies of small RNA accumulation and H3K9 methylation patterning on non-CG methylation, suggesting self-reinforcing mechanisms between these epigenetic factors. The results suggest that non-CG methylation patterns are critical in shaping the histone modification and small non-coding RNA landscapes.

2013-12-15 | GSE51304 | GEO

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)

| PRJNA576509 | ENA

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

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

| PRJNA508527 | ENA

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)

| PRJNA508528 | ENA

Non-CG methylation patterns shape the epigenetic landscape in Arabidopsis

2013-12-15 | E-GEOD-51304 | biostudies-arrayexpress

Cooperation between H3K27me3 and non-CG methylation in epigenetic regulation of genes in rice.

Project description:H3K27me3 is a repressive chromatin mark of genes and is catalyzed by homologs of Enhancer of zeste [E(z)], a component of Polycomb-repressive complex 2 (PRC2), while DNA methylation that occurs in CG and non-CG (CHG and CHH, where H is A, C or T) contexts is a hallmark of transposon silencing in plants. However, relationship between H3K27me3 and DNA methylation in gene repression remains unclear. In addition, the mechanism of PRC2 recruitment to specific genes is not known in plants. Here, we show that SDG711, a rice E(z) homolog, is required to maintain H3K27me3 of many developmental genes after shoot meristem to leaf transition and that many H3K27me3-marked developmental genes are also methylated at non-CG sites in the body regions. SDG711-binding and SDG711-mediated ectopic H3K27me3 also target genes methylated at non-CG sites. Conversely, mutation of OsDRM2, a major rice CHH methyltransferase, resulted in loss of SDG711-binding and H3K27me3 from many genes and their de-repression. Furthermore, we show that SDG711 physically interacts with OsDRM2 and a putative CHG methylation-binding protein. These results together suggest that the repression of many developmental genes may involve both DRM2-mediated non-CG methylation and PRC2-mediated H3K27me3 and that the two marks are not generally mutually exclusive but may cooperate in repression of developmentally regulated genes in rice.

2016-12-18 | GSE71640 | GEO

Genetic effects on non-CG DNA methylation

Project description:Genetic effects on non-CG DNA methylation

| PRJNA800436 | ENA