HiSeq Chip-seq analysis of whole genomic landscape of G9a and H3K9me2-targeted in CCICs
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE82131 | GEO | 2016/08/10
SECONDARY ACCESSION(S): PRJNA324111
REPOSITORIES: GEO
Similar Datasets
Project description:Purpose: to demonstrate that G9a maintain CCICs functional triats is independent of its methyltransferase activity. Method: ChIP-seq was applied to CCICs to elucidate the nature of G9a and H3K9me2-regulated differential gene targets by Illumina/Soleza Genome analyzer Results: It was shown that ghe 4,902 G9a-and H3K9me2-targeted genes are broadly idstributed throughout the genome, and both are co-localized at most of the sites in CCICs. G9a and H3K9me2-targeted in CCICs
2016-08-10 | E-GEOD-82131 | biostudies-arrayexpress
Project description:We profiled chromatin accessibility across the genome of HSPCs treated with either a small molecule inhibitor of G9a/GLP or DMSO. We observed that chromatin accessibility is dramatically altered at the regions of H3K9me2 nucleation. We have characterized the regions of H3K9me2 nucleation, revealing that H3K9me2 is nucleated in HSPCs at CpG islands (CGIs) and CGI-like sequences across the genome. Our analysis furthermore revealed a bias of H3K9me2 nucleation towards regions with low rates of C->T deamination, which typically lack DNA methylation. Lastly we examined the interaction of H3K9me2 and DNA methylation and determined that chromatin accessibility changes upon loss of H3K9me2 are dependent on the presence of DNA methylation. Examination of chromatin remodeling with FAIRE-seq in HSPCs treated with either a small molecule inhibitor of G9a/GLP or DMSO
2014-09-25 | E-GEOD-59749 | biostudies-arrayexpress
Project description:modENCODE_submission_5618 This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed. Developmental Stage: 3rd Instar Larvae; Genotype: G9a[RG5]/G9a[RG5]; Transgene: n/a; NUMBER OF REPLICATES: 4; EXPERIMENTAL FACTORS: Strain G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed. Antibody H3K9me2-Ab2 (new lot 3) (target is H3K9me2); Developmental Stage 3rd Instar Larvae
2013-03-13 | E-GEOD-45105 | biostudies-arrayexpress
Project description:The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify which genes were direct targets of G9a in hypertrophic cardiomyocytes, we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on cardiomyocytes isolated from normal mice (sham) and mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. We considered the best G9a-bound genomic regions as those in which G9a and H3K9me2 peaks overlapped. Since G9a contributes to trimethylation of H3K27 at a set of developmental genes through its interaction with PRC2, we also evaluated whether G9a had an effect on the distribution of this histone mark in hypertrophic cardiomyocytes. To this end, we performed ChIP-seq for H3K27me3 in CMs isolated from sham and TAC mice.
2017-08-30 | GSE93752 | GEO
Project description:We profiled chromatin accessibility across the genome of HSPCs treated with either a small molecule inhibitor of G9a/GLP or DMSO. We observed that chromatin accessibility is dramatically altered at the regions of H3K9me2 nucleation. We have characterized the regions of H3K9me2 nucleation, revealing that H3K9me2 is nucleated in HSPCs at CpG islands (CGIs) and CGI-like sequences across the genome. Our analysis furthermore revealed a bias of H3K9me2 nucleation towards regions with low rates of C->T deamination, which typically lack DNA methylation. Lastly we examined the interaction of H3K9me2 and DNA methylation and determined that chromatin accessibility changes upon loss of H3K9me2 are dependent on the presence of DNA methylation.
2014-09-25 | GSE59749 | GEO
Project description:We report the first genome-wide landscape of H3K9me2 ChIP-seq profile in mouse oocytes. We also performed whole-genome bisulfite sequencing and RNA-seq analysis of G9a conditional KO oocytes and maternal KO preimplantation embryos. Our findings illuminate the functional importance of G9a in preimplantation development and, in addition, pose a question on the proposed role for H3K9me2 in protection of the maternal genome from active CG demethylation.
2019-04-02 | GSE112320 | GEO
Project description:We have investigated the role of the histone methyltransferase G9a in the establishment of silent nuclear compartments. Following conditional knockout of the G9a methyltransferase in mouse ESCs, 167 genes were significantly up-regulated, and no genes were strongly down-regulated. A partially overlapping set of 119 genes were up-regulated after differentiation of G9a-depleted cells to neural precursors. Promoters of these G9a-repressed genes were AT rich and H3K9me2 enriched but H3K4me3 depleted and were not highly DNA methylated. Representative genes were found to be close to the nuclear periphery, which was significantly enriched for G9a-dependent H3K9me2. Strikingly, although 73% of total genes were early replicating, more than 71% of G9a-repressed genes were late replicating, and a strong correlation was found between H3K9me2 and late replication. However, G9a loss did not significantly affect subnuclear position or replication timing of any non-pericentric regions of the genome, nor did it affect programmed changes in replication timing that accompany differentiation. We conclude that G9a is a gatekeeper for a specific set of genes localized within the late replicating nuclear periphery. 4 cell states each in duplicate (i.e. a total of 8 individual replicates)
2010-06-20 | E-GEOD-18076 | biostudies-arrayexpress
Project description:We have investigated the role of the histone methyltransferase G9a in the establishment of silent nuclear compartments. Following conditional knockout of the G9a methyltransferase in mouse ESCs, 167 genes were significantly up-regulated, and no genes were strongly down-regulated. A partially overlapping set of 119 genes were up-regulated after differentiation of G9a-depleted cells to neural precursors. Promoters of these G9a-repressed genes were AT rich and H3K9me2 enriched but H3K4me3 depleted and were not highly DNA methylated. Representative genes were found to be close to the nuclear periphery, which was significantly enriched for G9a-dependent H3K9me2. Strikingly, although 73% of total genes were early replicating, more than 71% of G9a-repressed genes were late replicating, and a strong correlation was found between H3K9me2 and late replication. However, G9a loss did not significantly affect subnuclear position or replication timing of any non-pericentric regions of the genome, nor did it affect programmed changes in replication timing that accompany differentiation. We conclude that G9a is a gatekeeper for a specific set of genes localized within the late replicating nuclear periphery. 4 cell states each in duplicate (i.e. a total of 8 individual replicates)
2009-11-02 | E-GEOD-18079 | biostudies-arrayexpress
Project description:The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify the genomic regions bound to G9a in cardiomyocytes (CMs),we first generated a conditional, cardiac-specific KO mouse for this gene using the Cre-Lox approach, crossing G9a flox/flox mice with αMHC-MerCreMer mice (Cre mice were used as controls). Then we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on isolated G9a-KO and Cre CMs, and considered the best G9a-bound genomic regions as those that had a loss or decrease of G9a binding as well as a lower level of H3K9me2 in G9a-KO CMs. Since G9a contributes to trimethylation of H3K27 at a set of developmental genes through its interaction with PRC2, we also evaluated whether the loss of G9a had an effect on the distribution of this histone mark. To this end, we performed ChIP-seq for H3K27me3 in Cre CMs and G9a-KO CMs. Finally co-immunoprecipitation assays revealed that G9a interacts with Mef2c, thus to elucidate the function of the G9a–Mef2c interaction in adult cardiomyocytes, we used ChIP-seq to define the genomic distribution of Mef2c in Cre CMs and G9a-KO CMs.
2017-08-30 | GSE93690 | GEO
Project description:We have investigated the role of the histone methyltransferase G9a in the establishment of silent nuclear compartments. Following conditional knockout of the G9a methyltransferase in mouse ESCs, 167 genes were significantly up-regulated, and no genes were strongly down-regulated. A partially overlapping set of 119 genes were up-regulated after differentiation of G9a-depleted cells to neural precursors. Promoters of these G9a-repressed genes were AT rich and H3K9me2 enriched but H3K4me3 depleted and were not highly DNA methylated. Representative genes were found to be close to the nuclear periphery, which was significantly enriched for G9a-dependent H3K9me2. Strikingly, although 73% of total genes were early replicating, more than 71% of G9a-repressed genes were late replicating, and a strong correlation was found between H3K9me2 and late replication. However, G9a loss did not significantly affect subnuclear position or replication timing of any non-pericentric regions of the genome, nor did it affect programmed changes in replication timing that accompany differentiation. We conclude that G9a is a gatekeeper for a specific set of genes localized within the late replicating nuclear periphery.
2009-11-03 | GSE18079 | GEO