MNase-Seq for nucleosome occupancy
Ontology highlight
ABSTRACT:
ORGANISM(S): Oryza sativa
PROVIDER: GSE155267 | GEO | 2020/10/15
REPOSITORIES: GEO
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Project description:At genome-wide level, loss of OsChz1 causes mis-regulation of thousands of genes and broad alterations of nucleosome occupancy as well as reduction of H2A.Z-enrichment within chromatin along the gene body and at TSS. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H4K4me2), its loss does not affect the genome landscape of DNA methylation.
2020-10-15 | GSE155268 | GEO
Project description:At genome-wide level, loss of OsChz1 causes mis-regulation of thousands of genes and broad alterations of nucleosome occupancy as well as reduction of H2A.Z-enrichment within chromatin along the gene body and at TSS. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H4K4me2), its loss does not affect the genome landscape of DNA methylation.
2020-10-15 | GSE155266 | GEO
Project description:At genome-wide level, loss of OsChz1 causes mis-regulation of thousands of genes and broad alterations of nucleosome occupancy as well as reduction of H2A.Z-enrichment within chromatin along the gene body and at TSS. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H4K4me2), its loss does not affect the genome landscape of DNA methylation.
2020-10-15 | GSE155265 | GEO
Project description:At genome-wide level, loss of OsChz1 causes mis-regulation of thousands of genes and broad alterations of nucleosome occupancy as well as reduction of H2A.Z-enrichment within chromatin along the gene body and at TSS. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H4K4me2), its loss does not affect the genome landscape of DNA methylation.
2020-10-15 | GSE155264 | GEO
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| S-EPMC4859066 | biostudies-literature
Project description:Experiments performed over the past three decades have shown that nucleosomes are transcriptional repressors. In Saccharomyces cerevisiae, depletion of histone H4 results in the genome-wide transcriptional de-repression of hundreds genes. The mechanism of de-repression is hypothesized to be rooted directly in chromatin changes. To test this, we reproduced classical H4 depletion experiments by conditional repression of all histone H3 transcription, which depletes the supply of nucleosomes in vivo. RNA-seq results were consistent with the earlier studies, but much more sensitive, revealing nearly 2500 de-repressed genes. Changes in chromatin organization were determined by MNase-seq. Nucleosomes that were preferentially retained occurred in regions of high DNA-encoded nucleosome affinity, and were marked with H3K36me2, which is linked to transcription elongation. Nucleosomes harboring acetyl marks or that contained the variant histone H2A.z were preferentially lost. Genes that were de-repressed lost or rearranged nucleosomes at their promoter, but not in the gene body. Therefore, a combination of DNA-encoded nucleosome stability and nucleosome composition dictates which nucleosomes will be lost under conditions of limiting histone protein. This, in turn, governs which genes will experience a loss of regulatory fidelity. MNase-seq experiments consist of three wildtype (1 single-end and 2 paired-end) and four mutant (DCB200.1/H3 shutoff; 2 single-end, 2 paired-end) replicates. Each replicate contains two timepoints reflecting chromatin immediately after ("O hours") and 3 hours after transition to media containing dextrose. RNA-seq data includes three replicates from wildtype or H3 depleted cells after 3 hours in media containing dextrose.
2012-09-26 | E-GEOD-29291 | biostudies-arrayexpress
Project description:Open chromatin provides access to a wide spectrum of DNA binding proteins for DNA metabolism processes such as transcription, repair, recombination, and replication. In this regard, open chromatin profiling has been widely used to identify the location of regulatory regions, including promoters, enhancers, insulators, silencers, replication origins, and recombination hotspots. Regulatory DNA elements are made accessible by nucleosome-depeleted states. Thus, nucleosome remodelling and modification should be intimately coupled with open chromatin formation and regulation. However, our knowledge of nucleosome regulation is largely limited to promoter regions, which comprise only a subset of all regulatory loci in the genome. In order to examine nucleosome patterns in open chromatin regions, we performed micrococcal nuclease (MNase) sequencing for a laboratory strain of yeast. Nucleosome occupancy profiled by Micrococcal nuclease (MNase) digestion
2013-01-06 | E-GEOD-34923 | biostudies-arrayexpress
Project description:Open chromatin provides access to a wide spectrum of DNA binding proteins for DNA metabolism processes such as transcription, repair, recombination, and replication. In this regard, open chromatin profiling has been widely used to identify the location of regulatory regions, including promoters, enhancers, insulators, silencers, replication origins, and recombination hotspots. Regulatory DNA elements are made accessible by nucleosome-depeleted states. Thus, nucleosome remodelling and modification should be intimately coupled with open chromatin formation and regulation. However, our knowledge of nucleosome regulation is largely limited to promoter regions, which comprise only a subset of all regulatory loci in the genome. In order to examine nucleosome patterns in open chromatin regions, we performed micrococcal nuclease (MNase) sequencing for a laboratory strain of yeast.
2013-01-06 | GSE34923 | GEO
Project description:While it has been clearly established that well positioned H2A.Z-containing nucleosomes flank the nucleosome depleted region (NDR) at the transcriptional start site (TSS) of active mammalian genes, how this chromatin-based information is transmitted through the cell cycle is unknown. We show here that in trophoblast stem (TS) cells, the level of H2A.Z at promoters decreases during S phase coinciding with homotypic (H2A.Z/H2A.Z) nucleosomes flanking the TSS becoming heterotypic (H2A.Z/H2A). Surprisingly, these nucleosomes remain heterotypic at M phase. At the TSS, we identify an unstable heterotypic H2A.Z-containing nucleosome in G1 which, strikingly, is lost following DNA replication. These dynamic changes in H2A.Z at the TSS mirror a global expansion of the NDR at S and M which, unexpectedly, is unrelated to transcriptional activity. Coincident with the loss of H2A.Z at promoters, it is targeted to the centromere when mitosis begins We performed ChIP-Seq experiments (on mouse Trophoblast Stem cells arrested at G1; S and M stages of thecell cycle) using antibodies against histone variant H2A.Z and sequentional ChIP-re-ChIP-Seq experiments using H2A.Z antibody and H2A antibody in sequence. Combining those data sets with microarray gene expression expression data allowed us to see H2A.Z distribution over promoters of mouse coding genes in cell cycle dependant manner. Interestingly, Input also showed cell-cycle dependent effects, but histone H3 could be used as a cell-cycle independent normalisation factor. We also performed ChIP-seq with a CTCF pull-down to investigate its cell-cycle dependent relationship with heterochromatin.
2012-11-23 | E-GEOD-41371 | biostudies-arrayexpress