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DNA methylation, H3K4me2, H3K27me3, Pol2 promoter profiling during neuronal differentiation

ABSTRACT: Cellular differentiation entails loss of pluripotency and parallel gain of lineage-specific and ultimately cell-type specific characteristics. Using a murine system that progresses from stem cells to lineage-committed progenitors and further to terminally differentiated neurons we analyzed two repressive epigenetic pathways: DNA methylation and Polycomb-mediated methylation of histone H3 (H3K27me3). We show that several hundred promoters become DNA methylated in lineage-committed progenitor cells. Targets are selected for pluripotency and germline-specific genes, suggesting a role for DNA methylation in stabilizing loss of pluripotency already at the progenitor state. Conversely, we detect loss and acquisition of H3K27me3 at novel targets at both progenitor and terminal state. Surprisingly, many neuron-specific genes that are poised to be activated upon terminal differentiation become Polycomb targets only in progenitor cells. Moreover, promoters marked by H3K27me3 in stem cells frequently become DNA methylated during differentiation, suggesting context-dependent crosstalk between Polycomb and DNA methylation. This data suggest a new model how de novo DNA methylation and dynamic switches in Polycomb targets restrict pluripotency and define the developmental potential of progenitor cells. Keywords: MeDIP-chip, ChIP-chip, neuronal differentiation time-course

ORGANISM(S): Mus musculus

PROVIDER: GSE11489 | GEO | 2008/06/04

SECONDARY ACCESSION(S): PRJNA106419

REPOSITORIES: GEO

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DNA methylation, H3K4me2, H3K27me3, Pol2 promoter profiling during neuronal differentiation

Project description:Cellular differentiation entails loss of pluripotency and parallel gain of lineage-specific and ultimately cell-type specific characteristics. Using a murine system that progresses from stem cells to lineage-committed progenitors and further to terminally differentiated neurons we analyzed two repressive epigenetic pathways: DNA methylation and Polycomb-mediated methylation of histone H3 (H3K27me3). We show that several hundred promoters become DNA methylated in lineage-committed progenitor cells. Targets are selected for pluripotency and germline-specific genes, suggesting a role for DNA methylation in stabilizing loss of pluripotency already at the progenitor state. Conversely, we detect loss and acquisition of H3K27me3 at novel targets at both progenitor and terminal state. Surprisingly, many neuron-specific genes that are poised to be activated upon terminal differentiation become Polycomb targets only in progenitor cells. Moreover, promoters marked by H3K27me3 in stem cells frequently become DNA methylated during differentiation, suggesting context-dependent crosstalk between Polycomb and DNA methylation. This data suggest a new model how de novo DNA methylation and dynamic switches in Polycomb targets restrict pluripotency and define the developmental potential of progenitor cells. Keywords: MeDIP-chip, ChIP-chip, neuronal differentiation time-course MeDIP-chip and ChIP-chip experiments were performed with at least two independnet biological replicates. For each condition hybridizations include a dye-swap experiment.

2008-06-04 | E-GEOD-11489 | biostudies-arrayexpress

Chip-seq for H3K27me3 and H3K4me3 in DNA methylation deficient mouse embryonic fibroblasts

Project description:DNA methylation and the Polycomb Repression System are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear. By genome-wide mapping of the Polycomb Repressive Complex 2 (PRC2)-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and PRC2 from Polycomb-target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression. An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining PRC2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease. comparison of Dnmt1+/+ vs Dnmt1-/- mouse embryonic fibroblasts by ChIP-seq for H3K27me3 and H3K4me3

2013-02-20 | E-GEOD-44393 | biostudies-arrayexpress

Chip-chip for H3K27me3 and H3K4me3 in DNA methylation deficient mouse embryonic fibroblasts

2013-02-09 | E-GEOD-44149 | biostudies-arrayexpress

Comparison of gene expression in Dnmt1+/+ MEFs treated with 5-aza-2'-deoxycytidine or vector control

Project description:DNA methylation and the Polycomb Repression System are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear. By genome-wide mapping of the Polycomb Repressive Complex 2 (PRC2)-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and PRC2 from Polycomb-target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression. An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining PRC2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease. Two biological replicates are compared, each consisting of two technical replicates

2013-02-12 | E-GEOD-44276 | biostudies-arrayexpress

Comparison of gene expression in Dnmt1+/+ and Dnmt1-/- MEFs

2013-02-12 | E-GEOD-44277 | biostudies-arrayexpress

Reduced Representation Bisulfite Sequencing in DNA methylation deficient mouse embryonic fibroblasts

2013-03-01 | E-GEOD-44760 | biostudies-arrayexpress

mRNA-seq in DNA methylation deficient mouse embryonic fibroblasts

2013-03-01 | E-GEOD-44733 | biostudies-arrayexpress

Integrative proteomics reveals a protective role of PRC2 for the ground state pluripotent epigenome

Project description:The ground state of pluripotency is defined as a basal proliferative state free of epigenetic restriction, represented by mouse embryonic stem cells (ESCs) cultured with two kinase inhibitors (so-called “2i”). Through comparison with serum-grown ESCs, we identify epigenetic features characterizing 2i ESCs by proteome profiling of chromatin including post-translational histone modifications. The most prominent difference is H3K27me3 and its enzymatic writer complex PRC2 that are highly abundant on eu- and heterochromatin in 2i ESCs, with H3K27me3 redistributing outside canonical PRC2 targets in a CpG-dependent fashion. Using PRC2-deficient 2i ESCs, we identify epigenetic crosstalk with H3K27me3, including significant increases in H4 acetylation and DNA methylation. This suggests that the unique H3K27me3 configuration protects 2i ESCs from preparation to lineage priming. Interestingly, removal of DNA methylation in PRC2-deficient 2i ESCs lacking H3K27me3 using 5-azacytidine hardly affected ESC viability and transcriptome, showing that ESCs are independent of both major repressive epigenetic marks.

2018-11-21 | PXD007154 | Pride

DNA methylation profiling by HELP-seq in Dnmt1+/+ mouse embryonic fibroblasts

Project description:DNA methylation and the Polycomb Repression System are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear. By genome-wide mapping of the Polycomb Repressive Complex 2 (PRC2)-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and PRC2 from Polycomb-target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression. An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining PRC2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease. DNA methylation levels in Dnmt1+/+ mouse embryonic fibroblasts measured by HpaII tiny fragment Enrichment by Ligation-mediated PCR Sequencing (HELP-seq)

2013-03-01 | E-GEOD-44757 | biostudies-arrayexpress

Gain of function DNMT3A mutations cause microcephalic dwarfism and hypermethylation of Polycomb-regulated regions (mouse RRBS)

Project description:DNA methylation and Polycomb are key factors in the establishment of vertebrate cellular identity and fate. Here we report de novo missense mutations in DNMT3A, encoding the DNA methyltransferase DNMT3A, that cause microcephalic dwarfism, a hypocellular disorder of extreme global growth failure. Substitutions in the PWWP domain abrogate binding to the histone modifications H3K36me2/3, and alter DNA methylation in patient cells. Polycomb-associated DNA methylation canyons/valleys, hypomethylated domains encompassing developmental genes, become methylated with concomitant depletion of H3K27me3 and H3K4me3 bivalent marks. Such de novo DNA methylation occurs during differentiation of Dnmt3aW326R pluripotent cells in vitro, and is also evident in Dnmt3aW326R/+ dwarf mice. We therefore propose that the interaction of the DNMT3A PWWP domain with H3K36me2/3 normally limits DNA methylation of polycomb-marked regions. Our findings implicate the interplay between DNA methylation and polycomb at key developmental regulators as a determinant of organism size in mammals.

2018-11-26 | GSE120557 | GEO

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