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Distinct transcriptional outputs associated with mono- and di-methylated histone H3 arginine 2

ABSTRACT: Dimethylation of histone H3 arginine 2 (H3R2me2) maintains transcriptional silencing by inhibiting Set-1 mediated trimethylation of H3K4. Here we demonstrate that arginine 2 is also monomethylated (H3R2me1) in yeast but that its functional characteristics are distinct from H3R2me2: (a) H3R2me1 does not inhibit H3K4 methylation, (b) it is present throughout the coding region of genes and (c) it correlates with active transcription. Collectively, these results indicate that different H3R2 methylated states have defined roles in gene expression.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE14453 | GEO | 2009/01/20

SECONDARY ACCESSION(S): PRJNA111563

REPOSITORIES: GEO

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Distinct transcriptional outputs associated with mono- and di-methylated histone H3 arginine 2

Project description:Dimethylation of histone H3 arginine 2 (H3R2me2) maintains transcriptional silencing by inhibiting Set-1 mediated trimethylation of H3K4. Here we demonstrate that arginine 2 is also monomethylated (H3R2me1) in yeast but that its functional characteristics are distinct from H3R2me2: (a) H3R2me1 does not inhibit H3K4 methylation, (b) it is present throughout the coding region of genes and (c) it correlates with active transcription. Collectively, these results indicate that different H3R2 methylated states have defined roles in gene expression. hIP-chip analysis was performed to determine the genomic distribution of histone modifications H3R2me1, H3R2me2a, H3K4me3, H3K36me3, and H3K79me3 in the BY4741 yeast strain. ChIP samples were amplified, labelled, and hybridized to 50-mer tiling arrays covering the entire yeast genome at a 64 bp resolution.

2010-05-06 | E-GEOD-14453 | biostudies-arrayexpress

Arginine methylation at histone H3R2 controls deposition of H3K4 trimethylation

Project description:Modifications on histones control important biological processes through their effects on chromatin structure. Methylation at histone H3 lysine 4 (H3K4) by Set1p is found at the 5’end of active genes and contributes to transcriptional activation by recruiting chromatin remodeling enzymes. An adjacent arginine residue (H3R2) is also known to be asymmetrically dimethylated (H3R2me2a) in mammalian cells6, but its location within genes and its function in transcription are unknown. Here we show that H3R2 is also methylated in budding yeast. Using an antibody specific for H3R2me2a in ChIP-on-Chip analysis we determine the distribution of this modification on the entire yeast genome. We find that H3R2me2a is enriched at all heterochromatic loci, at inactive euchromatic genes and at the 3’-end of moderately transcribed genes. In all cases the pattern of H3R2 methylation is mutually exclusive with the presence of trimethylation at H3K4 (H3K4me3). The inverse correlation reflects the fact that methylation at H3R2 disrupts the ability of the Set1-complex to methylate H3K4. H3R2m2a inhibits specifically the trimethylation of H3K4 because it prevents Spp1 (a Set1-methyltranferase subunit) from binding to histone H3. These results indicate that methylation at H3R2 controls the global distribution of H3K4me3 and provides the first mechanistic insight into the function of arginine methylation on chromatin. Keywords: ChIP-chip

2007-07-31 | GSE8626 | GEO

Changes in protein arginine methylation by GSK3368712

Project description:Type I Protein Arginine Methyltransferases (PRMTs) catalyze asymmetric dimethylation of arginine residues on numerous proteins. Type I PRMTs and their substrates have been implicated in human cancers, suggesting that inhibiting Type I PRMT activity offers a tractable approach for therapeutic intervention. This dataset contains results from immunoproteomic studies enriching for monomethylated, asymmetrically, and symmetrically dimethylated arginines in cancer cell lines treated with the Type I PRMT inhibitor, GSK3368712.

2019-09-10 | PXD012747 | Pride

PRMT5: a Novel Regulator of Hepatitis B Virus Replication and an Arginine Methylase of HBV Core

Project description:In the study, we identified protein arginine methyltransferase 5 (PRMT5) as a novel restriction factor of HBV replication. We have also demonstrated that PRMT5 can interact with the HBV core and methylate its arginine residues within arginine-rich domain. We identified two types of HBc post-translational modifications: arginine methylation and ubiquitination. While monomethylated HBc retains cytoplasmic localization, symmetric dimethylation is linked to serine phosphorylation and nuclear transport. Thus arginine methylation and ubiquitination are novel types of HBc post-translational modifications which add another level of complexity to the understanding of HBc function and regulation of HBV replication

2017-11-01 | PXD006828 | Pride

Genome-wide maps of H3R2me2s in pro-B cells

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of H3R2me2s in mouse pro-B cells. We find that H3R2 symmetric dimethylation and H3K4 trimethylation colocalized throughout the genome of mouse pro-B cells. Examination of 2 different histone modifications in mouse pro-B cells

2012-02-02 | E-GEOD-35316 | biostudies-arrayexpress

Genome-wide maps of H3R2me2s in pro-B cells

2012-02-02 | GSE35316 | GEO

PHD finger recognition of unmodified histone H3R2 links UHRF1 to regulation of euchromatic gene expression

Project description:Histone methylation occurs on both lysine and arginine residues and its dynamic regulation plays a critical role in chromatin biology. Here we identify the UHRF1 PHD domain (PHDUHRF1), an important regulator of DNA CpG methylation, as an unanticipated histone H3 unmodified arginine 2 (H3R2)-recognition modality. This conclusion is based on binding studies and co-crystal structures of the PHDUHRF1 bound to histone H3 peptides, where the guanidinium group of unmodified R2 forms an extensive intermolecular hydrogen bond network, with methylation of H3R2, but not H3K4 or H3K9, disrupting complex formation. We have identified direct target genes of UHRF1 from microarray and ChIP studies. Importantly, we show that UHRF1’s ability to repress its direct target gene expression is dependent on PHDUHRF1 binding to unmodified H3R2, thereby demonstrating the functional importance of this recognition event and supporting the potential for crosstalk between histone arginine methylation and UHRF1 function. UHRF1 protein was depleted in HCT116 cells by shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The UHRF1-regulated genes were identified by comparing the gene expression profiles of control and UHRF1-depleted HCT116 cells.

2011-07-07 | E-GEOD-30478 | biostudies-arrayexpress

PHD finger recognition of unmodified histone H3R2 links UHRF1 to regulation of euchromatic gene expression

2011-07-07 | GSE30478 | GEO

Saccharomyces cerevisiae

Project description:Arginine methylation at histone H3R2 controls deposition of H3K4 trimethylation

| PRJNA101805 | ENA

Histone H3 Lysine 4 mono-, di- and trimethyl and CTCF in CD4+CD25+CD45RA+ regulatory and conventional CD4+CD25- T-cells

Project description:Analysis of Histone H3 Lysine 4 mono-, di- and trimethyl and the boundary protein CTCF in CD4+CD25+CD45RA+ regulatory T-cells and conventional CD4+CD25- T-cells. To investigate regulatory functions or potential new transcription start sites in Treg and Tconv cells, we investigated the associated histone modifications. Mono- and dimethylation of histone 3 lysin 4 (H3K4) were previously shown to mark enhancer regions, whereas H3K4 trimethylation generally associates with transcription start sites. At imprinted loci, binding of the insulator protein CTCF, which restricts or directs enhancer-promoter interactions, is often regulated by DNA-methylation. Therefore we performed ChIP-on-chip experiments (chromatin immunoprecipitation followed by microarray hybridization; samples were amplified with ligation mediated PCR [see label protocol for the procedure] prior to labeling) for mono- di- and trimethylation of histone 3 lysin 4 and of CTCF in expanded Treg and Tconv cells. Keywords: ChIP-on-chip ChIP-on-chip experiments for H3K4 mono-, di- and trimethyl and CTCF in CD4+CD25+CD45RA+ regulatory T-cells and conventional CD4+CD25- T-cells were co-hybridizied with the input. Three biologiacal replicates (rep1-3) were performed for every histone mark, two CTCF (rep1 and rep2).

2010-05-19 | E-GEOD-14234 | biostudies-arrayexpress

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