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Regulation and function of H3K36 di-methylation by the trithorax-group protein complex AMC

ABSTRACT: The goal of this study was to identify genes that are differentially expressed in animals that lack the histone methyltransferase Ash1 that generates H3K36 di-methylation

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE108120 | GEO | 2018/03/28

REPOSITORIES: GEO

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Regulation and function of H3K36 di-methylation by the trithorax-group protein complex AMC.

Project description: Not available

| S-EPMC5963871 | biostudies-other

Regulation and function of H3K36 di-methylation by the trithorax-group protein complex AMC

Project description:Regulation and function of H3K36 di-methylation by the trithorax-group protein complex AMC

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Mrg15 allosterically activates Ash1’s H3K36 methyltransferase activity and facilitates Ash1’s trithorax group protein function in Drosophila

Project description:Ash1 is a classic Trithorax group protein possessing an H3K36-specific histone methyltransferase activity. Ash1 plays a critical role in antagonizing Polycomb silencing and its loss-of-function mutations lead to inactivation of certain Hox genes and homeotic transformation. Here, we report the purification of Ash1 complex with the identification of two novel subunits, Mrg15 and Nurf55. Interestingly, Mrg15 stimulates the enzymatic activity of Ash1 in vitro, and such stimulation is independent of the chromo domain of Mrg15. In vivo, Mrg15 is recruited by Ash1 to their common target genes and Mrg15 is essential for the proper deposition of H3K36me2 at these regions.

2017-10-04 | GSE93100 | GEO

Trithorax-group protein ASH1 defines novel H3K36me3/H3K9me3 bivalent domains

Project description:A Trithorax-group (TrxG) protein ASH1 selectively dimethylates histone H3 lysine 36 (H3K36) and is required for expression of Hox genes. Genome-wide targets and molecular functions of ASH1, however, have remained elusive. Here we report ChIP-seq analysis of ASH1 targets in the human genome using a leukemia cell line K562. We identified 4,596 ASH1 binding sites, 2,502 of which are in the coding region, mostly in a proximity of promoters. Remaining half of the ASH1 binding sites are in the intergenic region. Analysis of histone methyation patterns revealed that a majority of ASH1 bidning sites are closely associated not only with trimethylated H3K36 (H3K36me3) but also with H3K9me3, shedding light for the first time to H3K36/H3K9 double methylation domains. Of note, an H3K9 methyltransferase SETDB1 is enriched in the ASH1 bidning sites, whereas EZH2 but not SUZ12 of the Polycomb Repression Complex 2 (PRC2) is present in bivalent domains. In addition, a small subset of ASH1 targets bear H3K4me3 and colocalize with RNA polymerase II. These select targets are highly enriched for regulators of gene expression, such as CXXC1, WHSC2/NELFA, and a battery of zinc finger proteins, suggesting that ASH1 might acts as a master regulator of gene expression.

2016-12-28 | GSE76145 | GEO

The role of H3K36 methylation and associated methyl transferases in chromosome-specific gene regulation

Project description:In Drosophila, two chromosomes require special mechanisms to balance their transcriptional output to the rest of the genome. These are the male-specific lethal complex targeting the male X chromosome and Painting of fourth targeting chromosome 4. Here, we explore the role of histone H3 methylated at lysine-36 (H3K36) and the associated methyltransferases—Set2, NSD, and Ash1—in these two chromosome-specific systems. We show that the loss of Set2 impairs the MSL complex–mediated dosage compensation; however, the effect is not recapitulated by H3K36 replacement and indicates an alternative target of Set2. Unexpectedly, balanced transcriptional output from the fourth chromosome requires intact H3K36 and depends on the additive functions of NSD and Ash1. We conclude that H3K36 methylation and the associated methyltransferases are important factors to balance transcriptional output of the male X chromosome and the fourth chromosome. Furthermore, our study highlights the pleiotropic effects of these enzymes.

2021-08-10 | GSE166934 | GEO

Analysis of the trithorax Group (trxG) genes ash2 and ash1 wing imaginal disc transcriptomes.

Project description:The absent, small or homeotic discs 2 (ash2) gene, a member of the trithorax Group (trxG) of transcriptional regulators, is functionally related to ash1. However, ASH2 and ASH1 belong to distinct multimeric complexes of unknown composition and it is unclear how they act to regulate transcription. In this study, examination of gene expression profiles in wing imaginal discs from ash2 and ash1 mutants revealed their transcriptomes are very similar and correlate with wing phenotypes. Keywords: loss of function analysis

2007-07-31 | GSE4923 | GEO

Set2-mediated H3K36 methylation states redundantly repress the production of antisense transcripts:: role in transcription regulation

Project description:Histone H3K36 can be added up to three methyl groups to form mono-, di-, and tri-methylation states. Recent study has shown that Set2 can suppress a specific group of antisense transcripts, which largely depends on the presence of H3K36 methylation. However, whether different methylation states possess distinct regulatory mechanisms on antisense transcripts is still unclear. In this study, we identified two yeast mutants that lack H3K36 di-methylation and tri-methylation, respectively. We also identified novel antisense transcripts in the absence of Set2 with own bioinformatics pipeline. Our study showed that the expression of these antisense transcripts does not affect the expression of corresponding sense genes. Different H3K36 methylation states (me2/me3) are not specific for the regulation of antisense expression, implying a co-regulation mechanism between them. Altogether, our study developed a method to identify new antisense transcripts, examined the potential effect of H3K36 di-methylation and tri-methylation on production of antisense transcripts. This study would shed light on the mechanism underlying how H3K36 methylation functions in the production of antisense transcripts.

2021-06-19 | GSE167338 | GEO

Histone H3K36 trimethylation is essential for multiple silencing mechanisms in fission yeast.

Project description:In budding yeast, Set2 catalyzes di- and trimethylation of H3K36 (H3K36me2 and H3K36me3) via an interaction between its SRI domain and C-terminal repeats of RNA polymerase II (Pol2) phosphorylated at Ser2 and Ser5 (CTD-S2,5-P). H3K36me2 recruits the Rpd3S histone deacetylase complex to repress cryptic transcription from transcribed regions. In fission yeast, Set2 is also responsible for H3K36 methylation, which represses a subset of RNAs including heterochromatic and subtelomeric RNAs, at least in part via recruitment of Clr6 complex II, a homolog of Rpd3S. Here, we show that CTD-S2Pâdependent interaction of fission yeast Set2 with Pol2 via the SRI domain is required for formation of H3K36me3, but not H3K36me2. H3K36me3 silenced heterochromatic and subtelomeric transcripts through post-transcriptional and transcriptional mechanisms, respectively, whereas H3K36me2 did not. Clr6 complex II appeared not to be responsible for heterochromatic silencing. Our results demonstrate that H3K36 methylation has multiple outputs in fission yeast; these findings provide insight into the multiple roles of H3K36 methylation in metazoans, which have different enzymes for synthesis of H3K36me1/2 and H3K36me3. Gene expression profile at exponentially-growing phase.in the fission yeast deletion mutants of set2.

2016-02-04 | E-GEOD-66821 | biostudies-arrayexpress

The trithorax group proteins Kismet and ASH1 promote H3K36 dimethylation to counteract Polycomb group repression in Drosophila.

Project description: Not available

| S-EPMC3787758 | biostudies-literature

Next Generation Sequencing of Two H3K36 methyltransferases during growth mycelia in the Magnaporthe oryzae

Project description:Di- and tri-methylation of lysine 36 on histone H3 (H3K36me2/3) are catalyzed by SET2 histone methyltransferase which play an important role in transcriptional elongation.we reveal a novel mechanism by which H3K36me2 and H3K36me3 associates with opposite transcriptional activity and Ash1 is required for the normal distribution of facultative heterochromatic modifications and stable maintenance of transcriptional silencing in eukaryotes.

2023-11-29 | GSE235261 | GEO

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