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H3K36me3 protects the mouse epigenome from single nucleotide variations [mRNA-Seq]

ABSTRACT: The goals of this project are to study the transcriptome profiling (RNA-seq) of mouse embryonic stem cells by histone mutants incorporation (H3.1K3M, H3.1K36M vs H3.1wt) or shRNA-mediated knockdown of methyl-transferase Suv39h1/h2 (shSuv39h1, shSuv39h2 vs shNC)

ORGANISM(S): Mus musculus

PROVIDER: GSE99155 | GEO | 2019/08/01

REPOSITORIES: GEO

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H3K36me3 protects the mouse epigenome from single nucleotide variations

Project description:We adopt histone H3 mutants competitive incorporation system to screen the effects of them on genetic fidelity. We find incorporation of H3K36M, an oncogenic histone mutant, produce a cancer or ageing-like genetic landscape by punctuating the H3K36me3/H3K9me3 dependent DNA repair mechanism. This work firstly get a direct relationship between epigenetic inheritance and genomic stability

2019-08-01 | GSE99156 | GEO

Histone H3.1K27 methylation promotes NHEJ by antagonizing FANCD2 on Chromatin

Project description:The goals of this project are to study the transcriptome profiling (RNA-seq) of human fribroblast cells undergoing H3K27me3 decrease by histone mutants incorporation (H3.1K27A/M vs H3.1wt) or shRNA-mediated knockdown of specific histone H3K27me3 methyl-transferase EZH2 (shEZH2 vs shNC)

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H3K36me3 protects the mouse epigenome from single nucleotide variations [CGH]

Project description:Copy numbers of mouse cells (ESCs and NIH3T3) carrying a series of single-site histone mutants or shRNAs comparing with control empty cells. Genomic DNA from candidate cells and control cells were respectively labeled by Cy5 or Cy3 and analyzed by array-based comparative genomic hybridization (aCGH).

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H3K36me3 protects the mouse epigenome from single nucleotide variations [ChIP-Seq]

Project description:We analyze high-throughput profiling of histone H3K36me3 in mouse embryonic stem cells from chromatin immunoprecipitated DNA captured by H3K36me3-specific antibody. We find that H3K36me3 distribution is like expected and enriched at transcribing gene bodies especially with enrichment at 3’-terminal of gene body, which is identical with findings observed in other mammalian cells.

2019-08-01 | GSE99154 | GEO

H3K36me3 protects the mouse epigenome from single nucleotide variations

Project description:H3K36me3 protects the mouse epigenome from single nucleotide variations

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Specificity, propagation and memory of pericentric heterochromatin in mouse fibroblasts

Project description:We assembled a quantitative map for the abundance and interactions of 16 factors related to PCH in living cells and found that stably bound complexes of the histone methyltransferase Suv39h1/2 demarcate the PCH state. From the experimental data we developed a predictive mathematical model that explains how chromatin-bound Suv39h1/2 complexes act as nucleation sites and propagate a spatially confined PCH domain with elevated histone H3 trimethylation levels via chromatin dynamics. Enrichment of HP1, Suv39h1/h2, H3K9me3 and H3K36me3 was assessed by ChIP-seq in NPCs derived from ESCs showing differential occupation at intergenic major satellite repeats and enrichment of heterochromatin factors. ChIP-seq of HP1, Suv39h1, Suv39h2, H3K9me3, H3K36me3 in NPCs

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DNA hypomethylation promotes UHRF1- and SUV39H1/H2-dependent crosstalk between H3K18ub and H3K9me3 to reinforce heterochromatin states [EPIC]

Project description:Mono-ubiquitination of lysine 18 on histone H3 (H3K18ub), catalyzed by UHRF1, is a DNMT1 docking site that facilitates replication-coupled DNA methylation maintenance. Its functions beyond this are unknown. Here, we genomically map simultaneous increases in UHRF1-dependent H3K18ub and SUV39H1/H2-dependent H3K9me3 following DNMT1 inhibition. Mechanistically, transient accumulation of hemi-methylated DNA at CpG islands facilitates UHRF1 recruitment and E3 ligase activity towards H3K18. Notably, H3K18ub enhances SUV39H1/H2 methyltransferase activity and, in colon cancer cells, nucleates new H3K9me3 domains at CpG island promoters of DNA methylation-silenced tumor suppressor genes. Disrupting UHRF1 enzyme activity prevents H3K9me3 accumulation while promoting PRC2-dependent H3K27me3 as a tertiary layer of gene repression in these regions. In contrast, disrupting H3K18ub-dependent SUV39H1/H2 activity enhances the transcriptional activating and antiproliferative effects of DNMT1 inhibition. Collectively, these findings reveal roles for UHRF1 and H3K18ub in regulating a hierarchy of repressive histone methylation signaling and rationalize a combination strategy for epigenetic cancer therapy.

2024-12-03 | GSE282922 | GEO

DNA hypomethylation promotes UHRF1- and SUV39H1/H2-dependent crosstalk between H3K18ub and H3K9me3 to reinforce heterochromatin states [RNA-Seq]

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DNA hypomethylation promotes UHRF1- and SUV39H1/H2-dependent crosstalk between H3K18ub and H3K9me3 to reinforce heterochromatin states [ChIP-Seq]

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DNA hypomethylation promotes UHRF1- and SUV39H1/H2-dependent crosstalk between H3K18ub and H3K9me3 to reinforce heterochromatin states

Project description:Mono-ubiquitination of lysine 18 on histone H3 (H3K18ub), catalyzed by UHRF1, is a DNMT1 docking site that facilitates replication-coupled DNA methylation maintenance. Its functions beyond this are unknown. Here, we genomically map simultaneous increases in UHRF1-dependent H3K18ub and SUV39H1/H2-dependent H3K9me3 following DNMT1 inhibition. Mechanistically, transient accumulation of hemi-methylated DNA at CpG islands facilitates UHRF1 recruitment and E3 ligase activity towards H3K18. Notably, H3K18ub enhances SUV39H1/H2 methyltransferase activity and, in colon cancer cells, nucleates new H3K9me3 domains at CpG island promoters of DNA methylation-silenced tumor suppressor genes. Disrupting UHRF1 enzyme activity prevents H3K9me3 accumulation while promoting PRC2-dependent H3K27me3 as a tertiary layer of gene repression in these regions. In contrast, disrupting H3K18ub- dependent SUV39H1/H2 activity enhances the transcriptional activating and antiproliferative effects of DNMT1 inhibition. Collectively, these findings reveal roles for UHRF1 and H3K18ub in regulating a hierarchy of repressive histone methylation signaling and rationalize a combination strategy for epigenetic cancer therapy.

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