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H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction [Agilent array]

ABSTRACT: We report that acetylation of H4K16 is a new marker of active enhancers and that some enhancers are marked by H3K4me1, MOF and H4K16ac but not by acetylated H3K27 or p300, suggesting that they are novel p300-independent regulatory elements.

ORGANISM(S): Mus musculus

PROVIDER: GSE47716 | GEO | 2013/08/23

SECONDARY ACCESSION(S): PRJNA207761

REPOSITORIES: GEO

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H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction [Agilent array]

Project description:We report that acetylation of H4K16 is a new marker of active enhancers and that some enhancers are marked by H3K4me1, MOF and H4K16ac but not by acetylated H3K27 or p300, suggesting that they are novel p300-independent regulatory elements. Gene expression in undifferentiated 46c (sox1-gfp) ES cells, and gfp FACS sorted cells after 5 days of differentiation to neural progenitor cells with NB27 and Neuro2 medium supplements. 3 biological replicates were performed for each sample.

2013-08-23 | E-GEOD-47716 | biostudies-arrayexpress

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction (I) [ChIP-Seq]

Project description:We report that acetylation of H4K16 is a new marker of active enhancers and that some enhancers are marked by H3K4me1, MOF and H4K16ac but not by acetylated H3K27 or p300, suggesting that they are novel p300-independent regulatory elements. ChIP-seq for H4K16 acetylation in undifferentiated ES cells, and cells after 3 days of retinoic acid differentiation, along with MNase digested input for both samples

2013-08-23 | E-GEOD-43102 | biostudies-arrayexpress

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction [NimbleGen array]

Project description:We report that acetylation of H4K16 is a new marker of active enhancers and that some enhancers are marked by H3K4me1, MOF and H4K16ac but not by acetylated H3K27 or p300, suggesting that they are novel p300-independent regulatory elements. ChIP on chip over neuronal and control genes for H4K16ac in undifferentiated 46c (sox1-gfp) ES cells and for 5 day differentiated FACS sorted Neural Progenitor Cells differentiated with NB27 and Neuro2 medium supplements

2013-08-23 | E-GEOD-47762 | biostudies-arrayexpress

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction [NimbleGen array]

2013-08-23 | GSE47762 | GEO

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction (II) [ChIP-Seq]

Project description:We report that acetylation of H4K16 is a new marker of active enhancers and that some enhancers are marked by H3K4me1, MOF and H4K16ac but not by acetylated H3K27 or p300, suggesting that they are novel p300-independent regulatory elements. ChIP-seq for H4K16 acetylation in undifferentiated 46c(sox1-gfp) ES cells, and FACS sorted day 5 Neural Progenitor Cells (differentiated with NB27 and Neuro2 medium supplements) , along with MNase digested input for both samples

2013-08-23 | E-GEOD-47761 | biostudies-arrayexpress

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction (I) [ChIP-Seq]

2013-08-23 | GSE43102 | GEO

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction (II) [ChIP-Seq]

2013-08-23 | GSE47761 | GEO

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction.

Project description: Not available

| S-EPMC3847775 | biostudies-literature

Upregulation of the mammalian X chromosome is associated with enhanced transcription initiation, MOF-mediated H4K16 acetylation, and longer RNA half-life

Project description:Many animal species employ a chromosome-based mechanism of sex determination, which has led to coordinate evolution of dosage compensation systems. Dosage compensation not only corrects the imbalance in the number of X-chromosomes between the sexes, but is also hypothesized to correct dosage imbalance within cells due to mono-allelic X expression and bi-allelic autosomal expression, by upregulating X-linked genes (termed M-bM-^@M-^XOhnoM-bM-^@M-^Ys hypothesisM-bM-^@M-^Y). To identify molecular mechanisms of X upregulation in mammals we established genome-wide profiles for the initiation and elongation forms of RNA polymerase II (PolII), PolII-S5p (phosphorylated at serine 5) and PolII-S2p (phosphorylated at serine 2), and for histone modifications in mouse cell lines and tissues. We found that in addition to being enriched in PolII-S5p but not in PolII-S2p, X-linked promoters were also enriched in two epigenetic marks, H4K16ac and H2AZ, dependent on expression levels. To address the function of the H4K16 acetyltransferase MOF occupancy profiles were established and knockdowns of MOF and MSL1 were done in mouse ES cells. Our results support a conserved role for the MSL complex to enhance transcription initiation of X-linked genes. Comparison of the profiles of RNA PolII, the H4K16ac acetyltransferase MOF and histone active marks on the X versus autosomes in mouse

2013-03-05 | E-GEOD-44835 | biostudies-arrayexpress

Selective binding of the PHD6 finger of MLL4 to histone H4K16ac links MLL4 and MOF

Project description:Histone methyltransferase MLL4 is centrally involved in transcriptional regulation and is often mutated in human diseases, including cancer and developmental disorders. MLL4 contains a catalytic SET domain that mono-methylates histone H3K4 and seven PHD fingers of unclear function. Here, we identify the PHD6 finger of MLL4 (MLL4-PHD6) as the first selective reader of the epigenetic modification H4K16ac. The solution NMR structure of MLL4-PHD6 in complex with a H4K16ac peptide along with binding and mutational analyses reveal unique mechanistic features underlying recognition of H4K16ac. Genomic studies show that one third of MLL4 chromatin binding sites overlap with H4K16ac-enriched regions in vivo and that MLL4 occupancy in a set of genomic targets depends on the acetyltransferase activity of MOF, a H4K16ac-specific acetyltransferase. The recognition of H4K16ac is conserved in the PHD7 finger of paralogous MLL3. Together, our findings highlight a novel acetyllysine reader and suggest that selective targeting of H4K16ac by MLL4 provides a direct functional link between MLL4, MOF and H4K16 acetylation.

2019-04-20 | GSE130091 | GEO

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