SLAM-seq on INTS11-degron cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE230124 | GEO | 2023/04/23
REPOSITORIES: GEO
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Project description:Here, we showed that acute lost H3K4me3 induces rapid reduction in global transcription with progressively increase in magnitude over the time-course cooccurrence with lost all H3K4 methylations. To further determine the effects of COMPASS subunits degradation on H3K4 methylations occupancies genome-wide, we performed time-course spike-in chromatin immunoprecipitation and sequencing (ChIP-seq, also known as ChIP-Rx) analysis in both degron systems.
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Project description:Here, we showed that acute lost H3K4me3 induces rapid reduction in global transcription with progressively increase in magnitude over the time-course cooccurrence with lost all H3K4 methylations,
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Project description:Here, we use elongation velocity analysis showed that acute loss INTS11 caused a general transcriptome-wide attenuation of elongation velocity in cells.
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Project description:Background: Previously we reported extensive gene expression reprogramming during epithelial to mesenchymal transition (EMT) of primary prostate cells. Here we investigated the hypothesis that specific histone and DNA methylations are involved in coordination of gene expression during EMT and early stages of transformation. Results: Genome-wide profiling of histone methylations (H3K4me3 and H3K27me3) and DNA methylation (DNAMe) was applied on a prostate cell model during EMT and malignant transformation. Integrated analyses of promoter epigenetic modifications and gene expression changes revealed strong correlations between the dynamic changes of histone methylations and gene expression. DNA methylation was weakly associated with global gene repression, but strongly correlated to gene silencing when genes co-modified by H3K4me3 were excluded. In genes labeled with multiple epigenetic marks in their promoters, the level of transcription was associated with the net signal intensity of the activating mark H3K4me3 minus the repressive mark H3K27me3 or DNAMe, indicating that the effect on gene expression of bivalent marks (H3K4/K27me3 or H3K4me3/DNAMe) depends on relative modification intensities. Sets of genes, including epithelial cell junction and EMT associated fibroblast growth factor receptor genes, showed corresponding changes concerning epigenetic modifications and gene expression during EMT. Conclusions: This work presents the first blueprint of epigenetic modifications during EMT in prostate cells and shows that specific histone methylations are extensively involved in gene expression reprogramming during EMT and carcinogenesis. The observation that transcription activity of bivalently marked genes depends on the relative labeling intensity of individual marks provides a new view of quantitative regulation of epigenetic modification.
2010-06-09 | E-TABM-983 | biostudies-arrayexpress
Project description:Background: Previously we reported extensive gene expression reprogramming during epithelial to mesenchymal transition (EMT) of primary prostate cells. Here we investigated the hypothesis that specific histone and DNA methylations are involved in coordination of gene expression during EMT and early stages of transformation. Results: Genome-wide profiling of histone methylations (H3K4me3 and H3K27me3) and DNA methylation (DNAMe) was applied on a prostate cell model during EMT and malignant transformation. Integrated analyses of promoter epigenetic modifications and gene expression changes revealed strong correlations between the dynamic changes of histone methylations and gene expression. DNA methylation was weakly associated with global gene repression, but strongly correlated to gene silencing when genes co-modified by H3K4me3 were excluded. In genes labeled with multiple epigenetic marks in their promoters, the level of transcription was associated with the net signal intensity of the activating mark H3K4me3 minus the repressive mark H3K27me3 or DNAMe, indicating that the effect on gene expression of bivalent marks (H3K4/K27me3 or H3K4me3/DNAMe) depends on relative modification intensities. Sets of genes, including epithelial cell junction and EMT associated fibroblast growth factor receptor genes, showed corresponding changes concerning epigenetic modifications and gene expression during EMT. Conclusions: This work presents the first blueprint of epigenetic modifications during EMT in prostate cells and shows that specific histone methylations are extensively involved in gene expression reprogramming during EMT and carcinogenesis. The observation that transcription activity of bivalently marked genes depends on the relative labeling intensity of individual marks provides a new view of quantitative regulation of epigenetic modification.
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Project description:H2B mono-ubiquitylation is required for multiple methylations of both H3K4 and H3K79 and has been implicated in gene expression from yeast to human. However, molecular crosstalk between H2BUb1 and other modifications, especially H3K4 and H3K79 methylations, remains unclear in vertebrates. To understand the functional role of H2BUb1, genome-wide histone modification patterns were measured in human cells. This study proposes dual roles of H2BUb1 that are both H3 methylation dependent and independent. First, H2BUb1 is a 5'-enriched active transcription mark and is co-occupied with H3K79 methylations in actively transcribed regions. Importantly, this study found a unique role of H2BUb1 in chromatin architecture independent of histone H3 methylations. H2BUb1 is well positioned in exon-intron boundaries of highly expressed exons and is specifically enriched in 5'-biased exons. Furthermore, H2BUb1 demonstrates increased occupancy in skipped exons compared to flanking exons for the human and mouse genome. Our findings suggest that a potentiating mechanism links H2BUb1 to both H3K79 methylations in actively transcribed regions and the exon-intron structure of highly expressed exons through the regulation of nucleosome dynamics during transcription elongation. We generated high-throughput sequencing (ChIP-seq) data for genome-wide occupancy of H2BUb1, nucleosome, H3K4me3, H3K36me3, H379me1/2/3, H3Ac, and mRNA in human embryonic carcinoma cells. We performed ChIP-seq for seven different histone modifications, MNase-seq, mRNA-seq (two replications), and inputDNA-seq in NCCIT cell lines (human embryonic carcinoma cell lines). We also performed mRNA-seq for RNF20-siRNA transfected NCCIT cells, where H2BUb1 signals decreased.
2012-03-07 | E-GEOD-25882 | biostudies-arrayexpress
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, 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. Our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.
2023-03-14 | PXD028858 | Pride
Project description:A hallmark of genes transcribed by RNA polymerase II (RNApII) is a "gradient" of histone H3 lysine 4 (H3K4) methylation. Various factors differentially bind to H3K4me3 near promoters, H3K4me2 just downstream, and H3K4me1 further downstream to modulate gene expression. Set1/COMPASS, the single S. cerevisiae H3K4 methyltransferase, binds transcribing RNApII, but COMPASS may also be allosterically regulated by specific subunits and histone H2B ubiquitylation. To ask whether differential H3K4 methylation is determined by regulated activity at specific gene locations or by the amount of time COMPASS spends near the nucleosome, ChIP-Seq analyses was performed in cells with altered transcription elongation rates or with Set1 fused to RNApII. Our results support a simple model where higher H3K4 methylations result from both increased duration and frequency of COMPASS proximity to the nucleosome.
2017-11-12 | GSE95356 | GEO