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Whole-genome landscape of histone H2AX and Î³-H2AX along with related factors in activated cells

ABSTRACT: Phosphorylation of the histone variant H2AX forms Î³-H2AX, which serves as a marker of DNA repair response. Here we provide ChIP-seq-based maps of histone H2AX, Î³-H2AX, H2AZ, INO80, SRCAP, and RNA polymerase II in activated T cells. Matched data for H2AX and Î³-H2AX in resting T cells and Jurkat cancer T cells are available in GSE25577. CD4+ T cells were stimulated in two different ways (IL-2 alone or IL-2 plus anti-CD3 and anti-CD28), and H2AX, Î³-H2AX, H2AZ, INO80, and SRCAP profiles were examined by ChIP-seq

ORGANISM(S): Homo sapiens

SUBMITTER: Jungmin Seo

PROVIDER: E-GEOD-44309 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide reorganization of histone H2AX toward particular fragile sites on cell activation.

Seo Jungmin J Kim Kwoneel K Chang Dong-Yeop DY Kang Ho-Bum HB Shin Eui-Cheol EC Kwon Jongbum J Choi Jung Kyoon JK

Nucleic acids research 20131024 2

γH2AX formation by phosphorylation of the histone variant H2AX is the key process in the repair of DNA lesions including those arising at fragile sites under replication stress. Here we demonstrate that H2AX is dynamically reorganized to preoccupy γH2AX hotspots on increased replication stress by activated cell proliferation and that H2AX is enriched in aphidicolin-induced replisome stalling sites in cycling cells. Interestingly, H2AX enrichment was particularly found in genomic regions that rep ...[more]

PMID: 24163101

Similar Datasets

Whole-genome landscape of histone H2AX and γ-H2AX along with related factors in activated cells

Project description:Phosphorylation of the histone variant H2AX forms γ-H2AX, which serves as a marker of DNA repair response. Here we provide ChIP-seq-based maps of histone H2AX, γ-H2AX, H2AZ, INO80, SRCAP, and RNA polymerase II in activated T cells. Matched data for H2AX and γ-H2AX in resting T cells and Jurkat cancer T cells are available in GSE25577.

2014-04-01 | GSE44309 | GEO

Whole-genome landscape of histone H2AX and M-NM-3-H2AX

Project description:Phosphorylation of the histone variant H2AX forms M-NM-3-H2AX that marks DNA double-strand break (DSB). Here we generated the sequencing-based maps of H2AX and M-NM-3-H2AX positioning in resting and proliferating cells before and after ionizing irradiation. Genome-wide locations of possible endogenous and exogenous DSBs were identified based on M-NM-3-H2AX distribution in dividing cancer cells without irradiation and that in resting cells upon irradiation, respectively. M-NM-3-H2AX-enriched regions of endogenous origin in replicating cells included telomeres and active transcription start sites, apparently reflecting replication- and transcription-mediated stress during rapid cell division. Surprisingly, H2AX itself, prior to phosphorylation, was specifically located at these endogenous hotspots. This phenomenon was only observed in dividing cancer cells but not in resting cells. Endogenous H2AX was concentrated on the transcription start site of actively transcribed genes but was irrelevant to pausing of RNA polymerase II (pol II), which precisely coincided with M-NM-3-H2AX of endogenous origin. M-NM-3-H2AX enrichment upon irradiation also coincided with actively transcribed regions, but unlike endogenous M-NM-3-H2AX, it extended into the gene body and was not specifically concentrated on the pausing site of pol II. Subtelomeres were not responsive to external DNA damage. Our findings provide insight into DNA repair programs of cancer and may have implications for cancer therapy. Profiles of H2AX and gamma-H2AX in normal resting and cancer T cells with and without ionizing irradiation.

2012-04-03 | E-GEOD-25577 | biostudies-arrayexpress

Genome wide profiling of the RNAPII, Î³H2AX, H3K4Me1, H3K4M2 and H3K4Me3 in MLL2 F/F and FC/FC MEF cells

Project description:We investigated the RNAPII and Î³H2AX occupancy genome wide by ChIP-Seq in MLL2 F/F and FC/FC80 MEF cells. We found that a week after MLL2 excision (FC/FC cells), a group of genes present higher levels of Î³H2AX and RNAPII near the TSS, as compared to the control (F/F cells). H3K4Me1, H3K4M2 and H3K4Me3 levels near the TSS were also studied. There is a total of 52 samples. 3 independent replicates for each experiment were performed. H3, H2AX and IgG ChIPs were used for normalisation or as controls.The experiments were performed using immortalised mouse embryonic fibroblasts (MEF) in which both MLL2 alleles were targeted by the loxp system (F/F cells). Tamoxifen treatment of the F/F cells for 24 hours results in the excision of both MLL2 alleles (FC/FC cells).

2016-04-13 | E-GEOD-73124 | biostudies-arrayexpress

Whole-genome landscape of histone H2AX and γ-H2AX

Project description:Phosphorylation of the histone variant H2AX forms γ-H2AX that marks DNA double-strand break (DSB). Here we generated the sequencing-based maps of H2AX and γ-H2AX positioning in resting and proliferating cells before and after ionizing irradiation. Genome-wide locations of possible endogenous and exogenous DSBs were identified based on γ-H2AX distribution in dividing cancer cells without irradiation and that in resting cells upon irradiation, respectively. γ-H2AX-enriched regions of endogenous origin in replicating cells included telomeres and active transcription start sites, apparently reflecting replication- and transcription-mediated stress during rapid cell division. Surprisingly, H2AX itself, prior to phosphorylation, was specifically located at these endogenous hotspots. This phenomenon was only observed in dividing cancer cells but not in resting cells. Endogenous H2AX was concentrated on the transcription start site of actively transcribed genes but was irrelevant to pausing of RNA polymerase II (pol II), which precisely coincided with γ-H2AX of endogenous origin. γ-H2AX enrichment upon irradiation also coincided with actively transcribed regions, but unlike endogenous γ-H2AX, it extended into the gene body and was not specifically concentrated on the pausing site of pol II. Subtelomeres were not responsive to external DNA damage. Our findings provide insight into DNA repair programs of cancer and may have implications for cancer therapy.

2012-04-04 | GSE25577 | GEO

High Mobility Group protein mediated transcription requires DNA damage marker Î³-H2AX

Project description:The eukaryotic genome is organized into chromatin, which constitutes the physiological template for DNA-dependent processes including replication, recombination, repair and transcription. Chromatin mediated transcription regulation involves histone modifications, chromatin remodeling and DNA methylation. However, the precise biological function of non-histone chromatin-associated proteins is still unclear. The high mobility group proteins are the most abundant non-histone chromatin-associated proteins. Here we combined proteomic, ChIP-seq and transcriptome data to decipher the mechanism of transcriptional regulation mediated by the high mobility group AT-hook protein 2 (HMGA2). We showed that HMGA2-induced transcription requires H2AX phosphorylation at S139 (H2AXS139ph; Î³-H2AX), mediated by the kinase ataxia telangiectasia mutated (ATM). Furthermore, we demonstrated the relevance of this mechanism within the biological context of TGFB1-signaling. Our results link H2AXS139ph, a marker for DNA damage, to transcription, which is a new function for this histone modification. The interplay between HMGA2, ATM and H2AX is a novel mechanism of transcription initiation. Chip-seq data of HMGA2, H2AXS139ph and ATM obtained from Mouse embryonic Fibroblast cells in wt and Ko of Hmga2

2015-11-04 | E-GEOD-63861 | biostudies-arrayexpress

H2AX controls motor learning and response to oxidative stress

Project description:ATM drives DNA repair through rapid phosphorylation of the histone variant H2AX. Similarities between ATM and H2AX are evident in the phenotypes of their knockout mouse models, but the role of H2AX in the brain remains obscure. Here, we provide the first evidence that H2AX loss leads to neurobehavioral deficits. H2AX regulates proper response to oxidative stress through Nrf2-transcriptional targets and treatment with antioxidant ameliorates the neurobehavioral deficits.

2018-03-09 | GSE102548 | GEO

Differentially expressed genes in H2AX knockdown cells undergoing apoptosis

Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear. To reveal the genes expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed genes in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.2-fold change and P-value ＜0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction.

2013-01-16 | GSE43498 | GEO

Differentially expressed miRNAs in H2AX knockdown cells undergoing apoptosis

Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear To reveal the miRNA expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed miRNAs in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.5-fold change and P-value ＜0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction.

2015-04-25 | GSE68233 | GEO

Differentially expressed genes in H2AX knockdown cells undergoing apoptosis

Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear. To reveal the genes expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed genes in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.2-fold change and P-value ï¼0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction. The two groups including control (C) and H2AX knockdown lung cancer cells (P1) were harvested 48 h after VP-16 treatment. Three independent experiments were performed for each group.

2013-01-16 | E-GEOD-43498 | biostudies-arrayexpress

Differentially expressed miRNAs in H2AX knockdown cells undergoing apoptosis

Project description:H2AX has been characterized as a novel tumor suppressor protein. Difficiency of H2AX will result in apoptotic inhibition of cancer cells. However, how H2AX epigenetically regulates apoptosis of cancer cells is still unclear To reveal the miRNA expression regulated by H2AX and involved in apoptosis, the microarray profiling analysis was employed to identify differentially expressed miRNAs in H2AX knockdown lung cancer cells and control ones after apoptotic induction. H2AX was knockdown by miRNA interfering system in human lung cancer originated cell A549 and the stable cell line named P1, while the control stable cell line named C. Genes with greater than 1.5-fold change and P-value ?0.05 were identified as differentially expressed genes between C and P1 cells both with apoptosis induction. The two groups including control (C) and H2AX knockdown lung cancer cells (P1) were harvested 48 h after VP-16 treatment. Three independent experiments were performed for each group.

2015-04-25 | E-GEOD-68233 | biostudies-arrayexpress

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