H2A.Z Mapping During G0/G1 and Mitosis
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE19568 | GEO | 2010/06/24
SECONDARY ACCESSION(S): PRJNA122475
REPOSITORIES: GEO
Similar Datasets
Project description:We report genome wide mapping of the histone variant H2A.Z during G0/G1 and mitosis in T24 bladder cancer cells. The results show that the broad enrichment pattern of H2A.Z near transcription start sites of active genes is maintained during mitosis. Furthermore, using H2A.Z localization to visualize nucleosome positioning near the start site, we see that the +1 nucleosome of active genes shifts upstream to occupy the transcription start sites during mitosis and the nucleosome depleted region is shortened. H2A.Z is also maintained on the -2 nucleosome which also shifts towrds the transcription start site during mitosis, further contributing to the shorteneing of the nucleosome depleted region. Examination of H2A.Z duing G0/G1 and mitosis in bladder cancer cells
2010-06-24 | E-GEOD-19568 | biostudies-arrayexpress
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
2012-11-23 | GSE41371 | 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
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 1,2, 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 surveyed whole genome expression using microarrays, in combination with H2A.Z ChIP-Seq (Illumina) data, to study the H2A.Z distribution on promoters of coding genes in different stages of the cell cycle in Trophoblast Stem (TS) cells. These data are published in Nekrasov et al., H2AZ inheritance during the cell cycle and it's impact on promoter organization and dynamics, Nature Structural and Molecular Biology (in press: accepted for publication on 24 Sep 2012).
2012-11-23 | GSE41370 | GEO
Project description:Nucleosomes that contain the histone variant H2A.Z are enriched around transcriptional start sites in many organisms. A single octameric nucleosome can contain two H2A.Z histones (homotypic) or one H2A.Z and one canonical H2A (heterotype). We generated high-resolution maps of homotypic and heterotypic Drosophila H2A.Z (H2Av) nucleosomes. Although homotypic and heterotypic H2Av nucleosomes map throughout most of the genome, homotypic nucleosomes are enriched and heterotypic nucleosomes are depleted downstream of active promoters and intron/exon boundaries. The distribution of homotypic H2A.Z nucleosomes resembles that of salt-soluble nucleosomes and shows evidence of displacement during transcriptional elongation. Homotypic nucleosomes are also depleted downstream of paused polymerases, where salt-soluble nucleosomes are conspicuously depleted. Our results suggest a model whereby H2A.Z enrichment patterns result from different structural interactions within the core of heterotypic and homotypic nucleosomes following disruption during transcriptional elongation. We analyzed two replicates for input, heterotypic and homotypic purifications. We sequenced one library for each of the single H2Av pulldown and 80mM salt soluble samples.
2010-11-01 | E-GEOD-21615 | biostudies-arrayexpress
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 1,2, 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 surveyed whole genome expression using microarrays, in combination with H2A.Z ChIP-Seq (Illumina) data, to study the H2A.Z distribution on promoters of coding genes in different stages of the cell cycle in Trophoblast Stem (TS) cells. These data are published in Nekrasov et al., H2AZ inheritance during the cell cycle and it's impact on promoter organization and dynamics, Nature Structural and Molecular Biology (in press: accepted for publication on 24 Sep 2012). Mouse Trophoblast stem (TS) cells were grown in cell culture medium. By adding specific drugs cells were arrested at particular stages of the cell cycle: G1; S and M. Total RNA was extracted from TS cells arrested at G1; S and M stages of cell cycle using TRizol (Invitrogen) extraction protocol and purified further the by RNAeasy Extraction Kit (Qiagen). RNA quality was assesed on Bioanalyzer total RNA chip. RNA samples were reverse transcribed and resulted cDNA samples were subjected to DNA microarray analysis (in triplicate) using the GeneChip Mouse Gene 1.0 ST Array (Affymetrix). Robust Multichip Average (RMA) correction and probe set summaries were obtained using Affymetrix Power Tools software annotation (Affymetrix) based on the mm9 mouse genome. Unless otherwise stated, all subsequent expression analyses (see Supplementary Methods) were performed in the R statistical computing environment (version 2.11.1).
2012-11-23 | E-GEOD-41370 | biostudies-arrayexpress
Project description:The histone variant H2A.Z is enriched in nucleosomes surrounding the transcription start site of active promoters, suggesting that it might be implicated in transcription. It is also required during mitosis. However, evidences obtained so far mainly rely on correlative evidences obtained in actively dividing cells. We have defined a paradigm in which cell cycle cannot interfere with H2A.Z transcriptional studies by developing an in vivo systems to invalidate H2A.Z in terminally differentiated post-mitotic muscle cells to dissociate its role during transcription from its role during mitosis. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is rather a marker than an actor of transcriptional activity.
2019-03-08 | GSE111575 | GEO
Project description:The histone variant H2A.Z is enriched in nucleosomes surrounding the transcription start site of active promoters, suggesting that it might be implicated in transcription. It is also required during mitosis. However, evidences obtained so far mainly rely on correlative evidences obtained in actively dividing cells. We have defined a paradigm in which cell cycle cannot interfere with H2A.Z transcriptional studies by developing an in vivo systems to invalidate H2A.Z in terminally differentiated post-mitotic muscle cells to dissociate its role during transcription from its role during mitosis. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is rather a marker than an actor of transcriptional activity.
2019-03-08 | GSE111573 | GEO
Project description:Here we compared the histone modification landscapes of mitotic and interphase cells to understand how histone modifications play a role in mitotic bookmarking. We found that the localization of histone modifications is maintained during mitosis, with methylation levels remaining the same, and acetylation levels decreasing. We found that at nucleosome depleted regions (NDRs), there is a nucleosome present during mitosis comprising a distinctive set of histone modifications, revealing a mitotic deposition and deacetylation of nucleosomes at NDRs.
2018-08-26 | GSE108173 | GEO
Project description:Nucleosomes that contain the histone variant H2A.Z are enriched around transcriptional start sites in many organisms. A single octameric nucleosome can contain two H2A.Z histones (homotypic) or one H2A.Z and one canonical H2A (heterotype). We generated high-resolution maps of homotypic and heterotypic Drosophila H2A.Z (H2Av) nucleosomes. Although homotypic and heterotypic H2Av nucleosomes map throughout most of the genome, homotypic nucleosomes are enriched and heterotypic nucleosomes are depleted downstream of active promoters and intron/exon boundaries. The distribution of homotypic H2A.Z nucleosomes resembles that of salt-soluble nucleosomes and shows evidence of displacement during transcriptional elongation. Homotypic nucleosomes are also depleted downstream of paused polymerases, where salt-soluble nucleosomes are conspicuously depleted. Our results suggest a model whereby H2A.Z enrichment patterns result from different structural interactions within the core of heterotypic and homotypic nucleosomes following disruption during transcriptional elongation.
2010-11-01 | GSE21615 | GEO