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Polycomb Repressor Complex 2 and REST-associated histone deacetylases are independent pathways toward a mature neuronal phenotype.

ABSTRACT: These experiments were designed to test the hypothesis that REST and Polycomb Repressor Complex 2 function cooperatively in undifferentiated ESCs. Our results showed that a majority of REST-bound genomic regions were not associated with H3K27me3 enrichment and loss of H3K27me3 enrichment was not a general observation in REST -/- ESCs. These results support the conclusion that REST and PRC2 function independently in ESCs and similarly contribute to maintaing a transcriptionally poised state through antagonism of H3K4me3. Examination of REST-bound regions in undifferentiated mouse embryonic stem cells (ESC), and a comparison of H3K27me3 distribution between WT and REST-/- ESCs.

ORGANISM(S): Mus musculus

SUBMITTER: Gail Mandel

PROVIDER: E-GEOD-48320 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Polycomb- and REST-associated histone deacetylases are independent pathways toward a mature neuronal phenotype.

McGann James C JC Oyer Jon A JA Garg Saurabh S Yao Huilan H Liu Jun J Feng Xin X Liao Lujian L Yates John R JR Mandel Gail G

eLife 20140924

The bivalent hypothesis posits that genes encoding developmental regulators required for early lineage decisions are poised in stem/progenitor cells by the balance between a repressor histone modification (H3K27me3), mediated by the Polycomb Repressor Complex 2 (PRC2), and an activator modification (H3K4me3). In this study, we test whether this mechanism applies equally to genes that are not required until terminal differentiation. We focus on the RE1 Silencing Transcription Factor (REST) becaus ...[more]

PMID: 25250711

Similar Datasets

Polycomb Repressor Complex2 and REST-associated histone deacetylases are independent pathways toward a mature neuronal phenotype

Project description:These experiments were designed to test the hypothesis that REST and Polycomb Repressor Complex 2 function cooperatively in undifferentiated ESCs. Our results show that H3K27me3-enriched genes show no de-repression in REST-/- ESCs, while REST target genes show significant de-repression. RNA-seq was performed and analyzed using two biological replicates for each genotype, WT (N6) and REST-/- (N8) mouse embryonic stem cells.

2014-09-30 | E-GEOD-59442 | biostudies-arrayexpress

Polycomb Repressor Complex 2 and REST-associated histone deacetylases are independent pathways toward a mature neuronal phenotype.

Project description:These experiments were designed to test the hypothesis that REST and Polycomb Repressor Complex 2 function cooperatively in undifferentiated ESCs. Our results showed that a majority of REST-bound genomic regions were not associated with H3K27me3 enrichment and loss of H3K27me3 enrichment was not a general observation in REST -/- ESCs. These results support the conclusion that REST and PRC2 function independently in ESCs and similarly contribute to maintaing a transcriptionally poised state through antagonism of H3K4me3.

2014-09-30 | GSE48320 | GEO

Polycomb Repressor Complex2 and REST-associated histone deacetylases are independent pathways toward a mature neuronal phenotype

Project description:These experiments were designed to test the hypothesis that REST and Polycomb Repressor Complex 2 function cooperatively in undifferentiated ESCs. Our results show that H3K27me3-enriched genes show no de-repression in REST-/- ESCs, while REST target genes show significant de-repression.

2014-09-30 | GSE59442 | GEO

ChIP-seq for Polycomb group proteins and H3K27me3 in ESCs and NSCs

Project description:ChIP-seq was performed for Ring1b, Ezh2, Cbx2 and H3K27me3 in ESCs and Ring1b and H3K27me3 in NSCs. This was used to define Polycomb-bound regions and to assess their H3.3 enrichment and turnover using time-ChIP.

2016-06-20 | GSE78899 | GEO

ATRX mutant neuroblastoma is sensitive to EZH2 inhibition via modulation of neuronal differentiation

Project description:We report on the characterization of ATRX in-frame fusion neuroblastoma and identify that ATRX IFF proteins re-locate from H3K9me3 enriched regions to active chromatin, such as the promoter of neural repressor REST. We further identify that REST is upregulated in ATRX IFF NB and that several neurogenesis and REST target genes are transcriptionally downregulated. Through ChIP-seq analysis, we observe that REST is bound to ATRX IFF Down genes, which have higher levels of H3K27me3. We further show that ATRX in-frame fusion neuroblastoma cells are sensitive to EZH2 inhibitors through de-repression of H3K27me3 bound neuronal function genes, includiing a subset of REST targets.

2019-10-15 | GSE100148 | GEO

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

Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

Project description:ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub). Two biological replicates were performed for Ring1B and H3K27me3 ChIPs in WT and Ring1B I53A/I53A mouse ESCs. Input chromatin was sequenced for each replicate as a control for ChIP enrichment.

2015-09-20 | E-GEOD-69955 | biostudies-arrayexpress

A comparative epigenomics approach reveals REST as a mediator of Polycomb reprogramming during neuronal differentiation

Project description:Transcription factors (TFs) in concert with chromatin pathways stably reset transcriptional programs during differentiation. Yet we know little how local sites of chromatin reprogramming are specified and how the estimated 3000 TF encoded in mammalian genomes contribute to chromatin dynamics. To identify candidate TFs we developed an integrated computational approach (Epi-MARA) that models chromatin dynamics in terms of predicted transcription factor binding sites and show that it correctly predicts key TFs involved in epigenome reorganization. When applied to a time course of genome-wide H3 lysine 27 trimethylation (H3K27me3), a chromatin mark set by the Polycomb system, during neuronal differentiation of murine stem cells Epi-MARA predicted that the repressive transcription factor REST contributes to a gain of H3K27me3 at a subset of promoters during the transition from the stem to the progenitor state. To test this prediction we identified, genome-wide, the actual binding sites of REST and H3K27me3 during the differentiation in cells that are either wildtype or in which REST had been deleted. REST indeed localizes to a subset of sites that gain H3K27me3 in progenitors. Importantly, absence of REST in trans leads to a loss of H3K27me3 predominantly in the neuronal progenitor state and specifically at those regions where REST was bound. This function further requires REST binding sites in cis as their mutation leads to substantial loss of H3K27me3. Taken together we provide a novel approach to identify epigenome and TF crosstalk during cellular reprogramming and prove experimentally the prediction that REST acts as an important recruiter of Polycomb repression during early steps of neurogenesis. Dataset comprises of 15 ChIP-seq samples using chromatin from embryonic stem (ES) and neuronal progentor (NP) of wildtype and RESTko cells, which was immunoprecipitated, using antibodies against REST, H3K27me3, or Suz12

2012-09-04 | E-GEOD-27148 | biostudies-arrayexpress

A comparative epigenomics approach reveals REST as a mediator of Polycomb reprogramming during neuronal differentiation

2012-09-04 | GSE27148 | GEO

Chd2 knockout effect on chromatin remodelling and the expression of developmental genes in mouse embryonic stem cells (RNA-Seq)

Project description:We demonstrate that chromodomain helicase DNA-binding domain 2 (Chd2) is required to maintain the differentiation potential of mouse ESCs. Chd2-depleted ESCs showed suppressed expression of developmentally regulated genes upon differentiation and subsequent differentiation defects without affecting gene expression in the undifferentiated state. Furthermore, chromatin immunoprecipitation followed by sequencing revealed alterations in a proportion of nucleosomes of developmentally regulated genes in Chd2-depleted ESCs to enhance histone variant H3.3 enrichment, leading to elevated trimethylation of histone H3 lysine 27.Chd2 is essential to prevent suppressive chromatin formation in developmentally regulated genes and determines subsequent effects on developmental processes in the undifferentiated state.

2017-05-15 | GSE96661 | GEO

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