Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A role for H3K4 mono-methylation in facultative heterochromatin assembly and partitioning of chromatin readers

ABSTRACT: Mono-methylation of lysine 4 on histone H3 (H3K4me1) is a well-established feature of enhancers and promoters, although its function is unknown. Remarkably, we find H3K4me1 at the promoter regions of conditionaly-repressed muscle and stimulus-dependent inflammatory response genes in myoblasts. During myogenesis, muscle genes are activated and become H3K4-trimethylated. On the promoters of active genes, we find that H3K4me1 spatially restricts the recruitment of “readers” of H3K4me3, including ING1, which, in turn, recruits Sin3A. Our findings point to a unique role for H3K4 mono-methylation in establishing boundaries that restrict the recruitment of chromatin-modifying enzymes to defined regions within promoters. Mapping of Wdr5, Menin, MLL1, Sin3A, and LSD1 in growing myoblasts (MB) and ING1 in growing myoblasts (MB) and fully differentiated myotubes (MT).

ORGANISM(S): Mus musculus

SUBMITTER: Roy Blum

PROVIDER: E-GEOD-50590 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

A role for H3K4 monomethylation in gene repression and partitioning of chromatin readers.

Cheng Jemmie J Blum Roy R Bowman Christopher C Hu Deqing D Shilatifard Ali A Shen Steven S Dynlacht Brian D BD

Molecular cell 20140301 6

Monomethylation of lysine 4 on histone H3 (H3K4me1) is a well-established feature of enhancers and promoters, although its function is unknown. Here, we uncover roles for H3K4me1 in diverse cell types. Remarkably, we find that MLL3/4 provokes monomethylation of promoter regions and the conditional repression of muscle and inflammatory response genes in myoblasts. During myogenesis, muscle genes are activated, lose MLL3 occupancy, and become H3K4-trimethylated through an alternative COMPASS compl ...[more]

PMID: 24656132

Similar Datasets

Genome-wide identification of enhancers in skeletal muscle

Project description:In an effort to identify the compendium of regulatory elements that govern myogenic differentiation, we generated chromatin state maps based on the recruitment of factors (p300 and PolII) and histone modifications (H3K4me1, H3K27ac) that typify enhancers in myoblasts and myotubes. We found a remarkable concordance between the location of these newly defined, active enhancers and MyoD1 binding events. In addition, we found a striking association between the position of enhancers and RNA polymerase II recruitment, which resulted in the expression of previously disclosed non-coding RNAs, as well as potentially new transcripts identified ab initio, throughout the enhancer region. Mapping of H3K27ac and p300 in growing myoblasts (MB) and fully differentiated myotubes (MT). Mapping of c-Jun in growing myoblasts (MB).

2012-12-15 | E-GEOD-37525 | biostudies-arrayexpress

Genome-wide remodeling of the epigenetic landscape during myogenic differentiation

Project description:We have examined changes in the chromatin landscape during muscle differentiation by mapping the genome-wide location of ten key histone marks and transcription factors in mouse myoblasts and terminally differentiated myotubes, providing an exceptionally rich dataset that has enabled discovery of key epigenetic changes underlying myogenesis. Using this compendium, we focused on a well-known repressive mark, histone H3 lysine 27 trimethylation, and identified novel regulatory elements flanking the myogenin gene that function as a key differentiation-dependent switch during myogenesis. Next, we examined the role of Polycomb-mediated H3K27 methylation in gene repression by systematically ablating components of both PRC1 and PRC2 complexes. Surprisingly, we found mechanistic differences between transient and permanent repression of muscle differentiation and lineage commitment genes and observed that the loss of PRC1 and PRC2 components produced opposing differentiation defects. These phenotypes illustrate striking differences as compared to embryonic stem cell differentiation and suggest that PRC1 and PRC2 do not operate sequentially in muscle cells. Our studies of PRC1 occupancy also suggested a "fail-safe" mechanism, whereby PRC1/Bmi1 concentrates at genes specifying nonmuscle lineages, helping to retain H3K27me3 in the face of declining Ezh2-mediated methyltransferase activity in differentiated cells. Mapping of PoII, H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3, H3K9Ac, H3K18Ac and H4K12Ac in growing myoblasts (MB) and fully differentiated myotubes (MT).

2011-05-08 | E-GEOD-25308 | biostudies-arrayexpress

A role for H3K4 mono-methylation in facultative heterochromatin assembly and partitioning of chromatin readers

Project description:Mono-methylation of lysine 4 on histone H3 (H3K4me1) is a well-established feature of enhancers and promoters, although its function is unknown. Remarkably, we find H3K4me1 at the promoter regions of conditionaly-repressed muscle and stimulus-dependent inflammatory response genes in myoblasts. During myogenesis, muscle genes are activated and become H3K4-trimethylated. On the promoters of active genes, we find that H3K4me1 spatially restricts the recruitment of “readers” of H3K4me3, including ING1, which, in turn, recruits Sin3A. Our findings point to a unique role for H3K4 mono-methylation in establishing boundaries that restrict the recruitment of chromatin-modifying enzymes to defined regions within promoters.

2014-03-29 | GSE50590 | GEO

Genome-wide maps of Sin3A and Sin3B binding in C2C12 myoblasts and differentiated myotubes

Project description:Sin3A and Sin3B bind to distinct and overlapping target sites. Sin3 proteins bind to distinct sites in cycling myoblasts whereas there is a converge of Sin3A and Sin3B proteins to sites in differentiated myotubes. We identified a subset of Sin3 target genes involved in muscle differentiation and physiology and showed that conditional ablation of Sin3 proteins in vivo in mouse results in sarcomere defects Examination of Sin3A and Sin3B binding during myogenesis

2011-01-01 | E-GEOD-22554 | biostudies-arrayexpress

Dynamic loss of H2B ubiquitylation without corresponding changes in H3K4 tri-methylation during myogenic differentiation

Project description:Ubiquitylation of H2B on lysine 120 (H2Bub) is associated with active transcriptional elongation. H2Bub has been implicated in histone cross-talk and is generally regarded to be a prerequisite for H3K4 and H3K79 tri-methylation in both yeast and mammalian cells. We performed a genome-wide analysis of epigenetic marks during muscle differentiation, and, strikingly, we observed a near-complete loss of H2Bub in the differentiated state. We examined the basis for global loss of this mark and found that the H2B ubiquitin E3 ligase, RNF20, was depleted from chromatin in differentiated myotubes, indicating that recruitment of this protein to genes substantially decreases upon differentiation. Remarkably, during the course of myogenic differentiation, we observed retention and acquisition of H3K4 tri-methylation on a large number of genes in the absence of detectable H2Bub. The Set1 H3K4 trimethylase complex was efficiently recruited to a subset of genes in myotubes in the absence of detectable H2Bub, accounting in part for H3K4 tri-methylation in myotubes. Our studies suggest that H3K4me3 deposition in the absence of detectable H2Bub in myotubes is mediated via Set1 and, perhaps, MLL complexes, whose recruitment does not require H2Bub. Thus, muscle cells represent a novel setting in which to explore mechanisms that regulate histone cross-talk. Mapping of H2Bub in growing myoblasts (MB) and fully differentiated myotubes (MT).

2012-03-06 | E-GEOD-34960 | biostudies-arrayexpress

Sex differences in the ventral tegmental area and nucleus accumbens proteome at baseline and following nicotine exposure

Project description:Sex differences in behaviors relevant to nicotine addiction have been observed in rodent models and human subjects. Behavioral, imaging and epidemiological studies also suggest underlying sex differences in mesolimbic dopamine signaling pathways. In this study we evaluated the proteome in the ventral tegmental area (VTA) and nucleus accumbens (NAc) shell in male and female mice. Experimental groups included two mouse strains (C3H/HeJ and C57BL/6J) at baseline, a sub-chronic, rewarding regimen of nicotine in C3H/HeJ mice, and chronic nicotine administration and withdrawal in C57BL/6J mice. Isobaric labeling with a TMT 10-plex system, sample fractionation, and tandem mass spectrometry were used to quantify changes in protein abundance. Similar or greater numbers of differentially regulated proteins were found between sexes at baseline in C3H/HeJ or C57BL/6J mice than within sexes following their respective regimen of nicotine administration. Despite differences by sex, strain, and nicotine exposure parameters, glial fibrillary acidic protein (GFAP) and dopamine and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32, Ppp1r1b) were repeatedly identified as significantly altered proteins, especially in the VTA. Further, network analyses showed sex- and nicotine-dependent regulation of a number of signaling pathways, including dopaminergic signaling. Sub-chronic nicotine exposure in female mice increased proteins related to dopaminergic signaling in the NAc shell but decreased them in the VTA, whereas the opposite pattern was observed in male mice. In contrast, dopaminergic signaling pathways were similarly upregulated in both male and female VTA after chronic nicotine and withdrawal. Overall, this study identifies significant sex differences in the proteome of the mesolimbic system, at baseline and after nicotine reward or withdrawal, which may help explain differential trajectories and susceptibility to nicotine addiction in males and females.

2021-06-28 | PXD023859 | Pride

RNA-sequencing of the mRNA transcriptome in lesional and non-lesional skin, across three time-points in severe psoriasis patients treated with the tumor necrosis factor (TNF) inhibitor, etanercept

Project description:Blood (mRNA and miRNA) and skin mRNA transcriptomes were investigated across three time-points in a pilot investigation of ten severe psoriasis patients, treated with the tumor necrosis factor (TNF) inhibitor, etanercept. We used illumina RNA-sequencing to analyse the small-RNA transcriptome in blood

2018-09-21 | E-MTAB-6556 | biostudies-arrayexpress

RNA-sequencing of the mRNA transcriptome in blood, across three time-points in severe psoriasis patients treated with the tumor necrosis factor (TNF) inhibitor, etanercept

2018-10-01 | E-MTAB-6555 | biostudies-arrayexpress

mRNA-seq analysis of superficial zone (SFZ) and deeper layers (deep AC) of articular cartilage of adult rats

Project description:We compared gene expression profiles of SFZ and deep AC of articular cartilage through laser microdissection (LMD) using adhesive tape, linear amplification of mRNA, and mRNA-seq analysis. gene expression profiles of SFZ and deep AC obtained from the proximal tibia of two adult rats

2014-05-08 | E-GEOD-57377 | biostudies-arrayexpress

A Seminavis robusta gene expression atlas

Project description:New RNA-seq data was generated to create a large-scale Seminavis robusta gene expression atlas profiling a wide-range of experimental conditions including life cycle stages and abiotic stressors. These stresses encompass among others changes in temperature and salt concentration, silica depletion, high light exposure, H202 and decadienal treatment.

2020-05-28 | E-MTAB-8685 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data