Genome-wide maps of H3 and H2A.Z RITE ChIP-sequencing
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ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE85031 | GEO | 2018/05/01
REPOSITORIES: GEO
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Project description:Genome-wide maps of H3 and H2A.Z RITE ChIP-sequencing
| PRJNA336001 | ENA
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:We use ChIP-Seq technology to profile the occupancy of histone H2A.Z and its chaperone in HeLa cells genome wide to check if they are co-colocalized. H2A.Z is ChIPed by antibody and its chaperone is tagged by Flag and ChIPed by M2 beads against Flag. ChIPed fragments are sequenced by Illumina HiSeq 2000 platform.
2014-03-01 | E-GEOD-52371 | 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: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:Here we report a novel role for H2A.Z.2 (H2AFV) as a mediator of cell proliferation and sensitivity to targeted therapies in malignant melanoma. While both H2A.Z.1 and H2A.Z.2 are highly expressed in metastatic melanoma and correlate with decreased patient survival, only H2A.Z.2 deficiency results in impaired cellular proliferation of melanoma cells, which occurs via a G1/S arrest. Integrated gene expression and ChIP-seq analyses revealed that H2A.Z.2 positively regulates E2F target genes, and that such genes acquire a distinct H2A.Z occupancy signature over the promoter and gene body in metastatic melanoma cells. We further identified the BET family member BRD2 as an H2A.Z-interacting protein in melanoma cells, and demonstrate that H2A.Z.2 silencing cooperates with BET inhibition to induce cell death. Cross-linked ChIP in SKmel147 melamoma cell line for E2F1 and BRD2
2015-07-01 | E-GEOD-68223 | biostudies-arrayexpress
Project description:Here we report a novel role for H2A.Z.2 (H2AFV) as a mediator of cell proliferation and sensitivity to targeted therapies in malignant melanoma. While both H2A.Z.1 and H2A.Z.2 are highly expressed in metastatic melanoma and correlate with decreased patient survival, only H2A.Z.2 deficiency results in impaired cellular proliferation of melanoma cells, which occurs via a G1/S arrest. Integrated gene expression and ChIP-seq analyses revealed that H2A.Z.2 positively regulates E2F target genes, and that such genes acquire a distinct H2A.Z occupancy signature over the promoter and gene body in metastatic melanoma cells. We further identified the BET family member BRD2 as an H2A.Z-interacting protein in melanoma cells, and demonstrate that H2A.Z.2 silencing cooperates with BET inhibition to induce cell death. Mononucleosomes from SK-mel147 (wt and stably expressing eGFP-H2A. eGFP-H2A.Z.1 and eGFP-H2A.Z.2) and melanocytes were isolated for ChIP with H2A.Z antibody or GFP trap beads (Chromotek).
2015-07-01 | E-GEOD-68222 | biostudies-arrayexpress
Project description:The histone variant H2A.Z plays key roles in gene expression, DNA repair, and centromere function. H2A.Z deposition is controlled by SWR-C chromatin remodeling enzymes that catalyze the nucleosomal exchange of canonical H2A with H2A.Z. Here we report that acetylation of histone H3 lysine 56 (H3-K56Ac) alters the substrate specificity of SWR-C, leading to promiscuous dimer exchange where either H2A.Z or H2A can be exchanged from nucleosomes. This result is confirmed in vivo, where genome-wide analysis demonstrates widespread decreases in H2A.Z levels in yeast mutants with hyperacetylated H3K56. Our work also suggests that a conserved SWR-C subunit may function as a M-bM-^@M-^\lockM-bM-^@M-^] that prevents removal of H2A.Z from nucleosomes. Our study identifies a histone modification that regulates a chromatin remodeling reaction and provides insights into how histone variants and nucleosome turnover can be controlled by chromatin regulators. H2A.Z ChIP seq experiments in mutants with constitutive H3K56ac
2013-04-15 | E-GEOD-43935 | biostudies-arrayexpress
Project description:To investigate the influence of the AtChz1A/B and ARP6 in H2A.Z incorporation, we analysed genome-wide H2A.Z density in the mutant and wild-type by ChIP-seq. We then performed H2A.Z occupancy analysis using data obtained from ChIP-seq of 3 different plants including mutants and wild-type.
2023-04-01 | GSE215800 | GEO