Genome-wide maps of H3K4me3 and H3K9me3 in SUN-depleted macrophages
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE107227 | GEO | 2022/11/01
REPOSITORIES: GEO
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Project description:Genome-wide maps of H3K4me3 and H3K9me3 in SUN-depleted macrophages
| PRJNA419370 | ENA
Project description:We used chromatin immunoprecipitation-coupled to deep sequencing (ChIP-seq) to profile genome-wide locations of H3K4 trimethylation (H3K4me3) and H3K27 trimethylation (H3K27me3) epigenetic marks in SATB1-depleted MDA-MB-231 aggressive breast cells.
2017-09-22 | GSE87169 | GEO
Project description:Epigenetic status has been linked to cardiac hypertrophy and heart failure. Histone deacetylase inhibitors are promising drugs for preventing cardiac remodeling. We previously demonstrated very different patterns of histone H3 lysine 9 trimethylation (H3K9me3) and histone H3 lysine 4 trimethylation (H3K4me3) in failing hearts compared to control hearts in both animal models and clinical heart specimens. Here, we focused on a heart failure-specific histone modification, H3K9me3, and investigated the prognostic efficacy of administering a histone H3K9 methyltransferase inhibitor, chaetocin, to Dahl salt-sensitive rats, an animal model of heart failure. Chaetocin delayed the timing of transition from cardiac hypertrophy to heart failure, and prolonged survival in this animal model. Mitochondrial dysfunction was improved with inhibitor use in the failing heart. ChIP-seq analysis demonstrated that heart failure caused an increase in H3K9me3 alignments in thousands of repetitive elements, including regions neighboring mitochondrial genes, and a corresponding reduction of this effect with inhibitor use. However, at 35 loci, heart failure was conversely associated with a reduction in H3K9me3 alignments, and inhibitor use reversed this effect. These data suggest that excessive heterochromatinization of repetitive elements in the failing heart might impair pumping function with mitochondrial gene silencing. H3K9 methyltransferase inhibitors may be a promising novel therapy for chronic heart failure.
2015-05-31 | GSE69194 | GEO
Project description:The importance of germline-inherited posttranslational histone modification in priming early mammalian development is just emerging1-4. Histone H3 lysine 9 (H3K9) trimethylation is associated with heterochromatin and gene repression during cell-fate change5, while histone H3 lysine 4 (H3K4) trimethylation marks active gene promoters6. Mature oocytes are transcriptionally quiescent and possess remarkably broad domains of H3K4me3 (bdH3K4me3)1, 2. It remains unknown, which factors contribute to the maintenance of the bdH3K4me3 landscape. Lysine-specific demethylase 4A (KDM4A) demethylates H3K9me3 at promoters marked by H3K4me3 in actively transcribing somatic cells7. Here, we report that KDM4A-mediated H3K9me3 demethylation at bdH3K4me3 in oocytes is crucial for normal preimplantation development and zygotic genome activation (ZGA) after fertilization. Loss of KDM4A in oocytes causes extensive and aberrant H3K9me3 spreading at bdH3K4me3, resulting in insufficient transcriptional activation ZGA genes, endogenous retroviral elements and long terminal repeat -initiated chimeric transcripts in 2-cell embryos. The catalytic activity of KDM4A is essential for normal epigenetic reprogramming and preimplantation development. Hence, KDM4A plays a crucial role in preserving maternal epigenome integrity required for proper ZGA and transfer of developmental control to the embryo.
| EGAS00001004220 | EGA
Project description:PTEN, a widely investigated tumor suppressor, has at least two longer translational variants, PTEN and . However, the regulation and precise roles of endogenous PTEN/ in tumorigenesis remain greatly unknown. Here we show that USP9X and FBXW11 selectively regulate the stability of PTEN/ but not PTEN proteins by deubiqitination and ubiquitination respectively. USP9X promotes and FBXW11 suppresses tumorigenesis mediated by PTEN/. In contrast to the current paradigm for PTEN as a tumor suppressor, PTEN/ promote tumorigenesis of cancer cells in a phosphatase-independent manner. Mechanistically, PTEN/ localized in the nucleus regulate expressions of tumor-promoting genes such as NOTCH3 in the similar way as the H3K4 presenter WDR5. Further, PTEN/ but not PTEN directly interact with WDR5 to promote trimethylation of H3K4 and maintain a tumor-promoting signature. Taken together, our results indicate that PTEN/ are a double-edged sword for carcinogenesis, suggesting that reinterpretation of the importance of PTEN gene in carcinogenesis is warranted.
2019-11-14 | PXD013196 | Pride
Project description:In this study we explored the effects of chronological and photoageing on the miRNome of human skin. To this end, miRNA expression was analysed in biopsies collected from sun-exposed (outer arm) and sun-protected (inner arm) skin from fair-skinned (phototype II/III) healthy female volunteers of two age groups: young, 18-25 years and aged, >70 years. Strict inclusion criteria were used for photoageing scoring and for chronological ageing. Microarray analysis revealed that chronological ageing had minor effect on the human skin miRNome. In contrast, photoageing had a robust impact on miRNAs, and a set of miRNAs differentially expressed between sun-protected and sun-exposed skin of the young and aged groups was identified. We have performed miRNome analysis (using microarray) on RNA isolated from sun-exposed and sun-protected skin of young and old females
2018-08-31 | GSE114006 | GEO
Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and proposed to regulate transcription initiation. However, redundant functions of the H3K4 SET1/COMPASS methyltransferase complexes complicate elucidation of the specific role of H3K4me3 in transcriptional regulation. Here, by using mouse embryonic stem cells (mESCs) as a model system, we show that acute ablation of shared subunits of the SET1/COMPASS complexes leads to complete loss of all H3K4 methylation. H3K4me3 turnover occurs more rapidly than H3K4me1 and H3K4me2 and is dependent on KDM5 demethylases. Surprisingly, acute loss of H3K4me3 does not have detectable effects on transcriptional initiation but leads to a widespread decrease in transcriptional output, an increase in RNA polymerase II (RNAPII) pausing and slower elongation. Notably, we show that H3K4me3 is required for the recruitment of the Integrator Complex Subunit 11 (INTS11), which is essential for the eviction of paused RNAPII and transcriptional elongation. Thus, our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.
2023-02-10 | PXD039176 | Pride
Project description:In yeast and other eukaryotes, the histone methyltransferase Set1 mediates methylation of lysine 4 on histone H3 (H3K4me). This modification marks the 5' end of transcribed genes in a 5' to 3' tri- to di- to monomethyl gradient, and promotes association of chromatin remodeling enzymes that regulate transcription. In a screen to identify factors that control the distinct H3K4 methylation states, we identified Ctk1, the serine 2 C-terminal domain (CTD) kinase for RNA polymerase II (RNAP II). We found that CTK1 deletion nearly abolished H3K4 monomethylation, yet caused a significant increase in H3K4 di- and trimethylation. Both on individual genes and genome-wide, the loss of CTK1 disrupted the H3K4 methylation patterns normally observed. H3K4me2 and H3K4me3 spread 3' into the body of genes, while H3K4 monomethylation was diminished. These effects were dependent on the catalytic activity of Ctk1, but are independent of Set2-mediated H3K36 methylation. Furthermore, these effects are not due to spurious transcription initiation in the body of genes, changes in RNAP II occupancy, changes in serine 5 CTD phosphorylation patterns, or to ‘transcriptional stress’. These data show that Ctk1 acts to restrict the spread of H3K4 methylation through a mechanism that is independent of a general transcription defect. The evidence presented indicates that Ctk1 controls the maintenance of suppressive chromatin in the coding regions of genes by both promoting H3K36 methylation, which leads to histone hypoacetylation, and by preventing the 3' spread of H3K4 trimethylation, a mark associated with chromatin remodeling at the 5' end of genes. Keywords: ChIP-chip
2006-11-01 | GSE5572 | GEO
Project description:We report the difference of genome-wide chromatin profiling of histone modifications in mammalian cells after PBS or LPS treatment. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse peritoneal macrophages. We find that lysine 4 and lysine 9 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential.Trimethylation of lysine 9 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of mammalian cells after LPS treatment.
2019-08-04 | GSE102252 | GEO
Project description:Genome wide DNA methylation profiling of epidermal and dermal samples obtained from sun-exposed and sun-protected body sites from younger (<35 years old) and older (>60 years old) individuals. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in dermal and epidermal samples. Samples included 10 younger sun protected dermal samples, 10 younger sun exposed dermal samples, 10 older sun protected dermal samples, 10 older sun exposed dermal samples, 9 younger sun protected epidermal samples, 9 younger sun exposed epidermal samples, 10 older sun protected epidermal sample, 10 older sun exposed epidermal samples.
2015-03-23 | GSE51954 | GEO