EGAS00001004660_WGBS - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001006538 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:RNA data for EGAS00001004660, "Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin"
| EGAD00001006539 | EGA
Project description:Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin
| PRJNA680038 | ENA
Project description:Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin. [Expression profile of human PDAC primary cells]
| PRJNA553762 | ENA
Project description:Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin [EPIC methylation data on cell lines and PDXs]
| PRJNA554343 | ENA
Project description:Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin. [Activation of stellate cells by tumor conditioned medium]
| PRJNA553765 | ENA
Project description:In mammals, DNA methylation is essential for protecting repetitive sequences from aberrant transcription, translocation, and homologous recombination. However, DNA hypomethylation occurs during specific developmental stages (e.g. preimplantation embryos) and in certain cell types (e.g., primordial germ cells). The absence of dysregulated repetitive elements in these cells suggests the existence of alternative mechanisms that prevent genome instability triggered by DNA hypomethylation. In this report, we seek to elucidate the factors that play a critical role in ensuring genome stability by focusing on DAXX and ATRX, two proteins that have been linked to transcriptional control and epigenetic regulation. We carried out ChIP-seq and RNA-seq analyses to compare the genome-wide binding and transcriptome profiles of DAXX and ATRX in mouse ES (mES) cells triple knocked out for the three mammalian DNA methyltransferases (DNMTs) (TKO cells) to those in wildtype mES cells. Our data indicate that DAXX and ATRX are distinct in their chromatin-binding profiles and highly co-enriched at tandem repetitive elements. Global DNA hypomethylation, as was the case in TKO cells, further promoted the recruitment of the DAXX/ATRX complex to tandem repeat sequences including IAP (intracisternal A‐particle) retrotransposons and telomeres. Inhibition of DAXX or ATRX in cells with hypomethylated genomes (e.g., TKO cells, mES cells cultured in ground-state conditions, and preimplantation embryos) increased aberrant transcriptional de-repression of repeat elements and dysfunction at telomeres. Furthermore, we provide evidence that DAXX/ATRX-dependent silencing may occur through DAXX’s interaction with SUV39H1 and increased H3K9me3 on repetitive sequences. Our study suggests that DAXX and ATRX are important for safeguarding the genome, particularly in silencing repetitive elements in the absence of DNA methylation. We tested the hypothesis that the DAXX/ATRX complex participates in protecting repetitive elements in the absence of DNA methylation. To this end, we investigated genome-wide chromatin targeting of DAXX and ATRX in wildtype mES cells, and in mES cells that exhibit extensive loss of DNA methylation due to homozygous knockout of all three DNA.
2015-07-15 | E-GEOD-70811 | biostudies-arrayexpress
Project description:Inflammation is an established feature of many age-related diseases, and growing evidence implicates transcripts from repetitive elements in inflammatory signaling with aging. We generated transcriptomic (RNA-seq) and whole-genome bisulfite sequencing (WGBS, for methylation) data on frozen/biobanked peripheral blood mononuclear cells from middle-aged and older adults, as well as younger and older adults before and after an exercise intervention, to evaluate correlations among repetitive elements and inflammation, along with methylation of repetitive elements.
2024-04-09 | GSE263013 | GEO
Project description:In mammals, DNA methylation is essential for protecting repetitive sequences from aberrant transcription, translocation, and homologous recombination. However, DNA hypomethylation occurs during specific developmental stages (e.g. preimplantation embryos) and in certain cell types (e.g., primordial germ cells). The absence of dysregulated repetitive elements in these cells suggests the existence of alternative mechanisms that prevent genome instability triggered by DNA hypomethylation. In this report, we seek to elucidate the factors that play a critical role in ensuring genome stability by focusing on DAXX and ATRX, two proteins that have been linked to transcriptional control and epigenetic regulation. We carried out ChIP-seq and RNA-seq analyses to compare the genome-wide binding and transcriptome profiles of DAXX and ATRX in mouse ES (mES) cells triple knocked out for the three mammalian DNA methyltransferases (DNMTs) (TKO cells) to those in wildtype mES cells. Our data indicate that DAXX and ATRX are distinct in their chromatin-binding profiles and highly co-enriched at tandem repetitive elements. Global DNA hypomethylation, as was the case in TKO cells, further promoted the recruitment of the DAXX/ATRX complex to tandem repeat sequences including IAP (intracisternal A‐particle) retrotransposons and telomeres. Inhibition of DAXX or ATRX in cells with hypomethylated genomes (e.g., TKO cells, mES cells cultured in ground-state conditions, and preimplantation embryos) increased aberrant transcriptional de-repression of repeat elements and dysfunction at telomeres. Furthermore, we provide evidence that DAXX/ATRX-dependent silencing may occur through DAXX’s interaction with SUV39H1 and increased H3K9me3 on repetitive sequences. Our study suggests that DAXX and ATRX are important for safeguarding the genome, particularly in silencing repetitive elements in the absence of DNA methylation.
2015-07-15 | GSE70811 | GEO
Project description:In mammals, DNA methylation is essential for protecting repetitive sequences from aberrant transcription, translocation, and homologous recombination. However, DNA hypomethylation occurs during specific developmental stages (e.g. preimplantation embryos) and in certain cell types (e.g., primordial germ cells). The absence of dysregulated repetitive elements in these cells suggests the existence of alternative mechanisms that prevent genome instability triggered by DNA hypomethylation. In this report, we seek to elucidate the factors that play a critical role in ensuring genome stability by focusing on DAXX and ATRX, two proteins that have been linked to transcriptional control and epigenetic regulation. We carried out ChIP-seq and RNA-seq analyses to compare the genome-wide binding and transcriptome profiles of DAXX and ATRX in mouse ES (mES) cells triple knocked out for the three mammalian DNA methyltransferases (DNMTs) (TKO cells) to those in wildtype mES cells. Our data indicate that DAXX and ATRX are distinct in their chromatin-binding profiles and highly co-enriched at tandem repetitive elements. Global DNA hypomethylation, as was the case in TKO cells, further promoted the recruitment of the DAXX/ATRX complex to tandem repeat sequences including IAP (intracisternal A‐particle) retrotransposons and telomeres. Inhibition of DAXX or ATRX in cells with hypomethylated genomes (e.g., TKO cells, mES cells cultured in ground-state conditions, and preimplantation embryos) increased aberrant transcriptional de-repression of repeat elements and dysfunction at telomeres. Furthermore, we provide evidence that DAXX/ATRX-dependent silencing may occur through DAXX’s interaction with SUV39H1 and increased H3K9me3 on repetitive sequences. Our study suggests that DAXX and ATRX are important for safeguarding the genome, particularly in silencing repetitive elements in the absence of DNA methylation.
2015-07-15 | GSE70849 | GEO
Project description:Multiple myeloma (MM) is a malignant plasma cell tumor characterized by various chromosomal aberrations. From the aspect of epigenetics, hypomethylation of DNA repetitive elements has been considered to induce chromosomal instability. We therefore have been interested in how it is related to chromosomal aberrations in MM. To address this, methylation levels of repetitive elements (including LINE-1, Alu and Satellite-alpha) and copy number alterations were measured in clinical samples (N=85). Bisulfite-pyrosequencing (N=85) and array-based comparative genomic hybridization (N=73) were used for these measurement, respectively. As results, methylation levels of repetitive elements were linearly associated with the degree of malignancy of plasma cells. Combined with hierarchical clustering of the result of aCGH, hypomethylation of repetitive elements was well associated with frequent chromosomal deletions. In particular, methylation levels of LINE-1 was significantly higher in samples with chromosome 13 deletion than the other (36.1% vs. 44.0%, P=0.010). The number of deleted probes was significantly correlated with LINE-1 methylation levels (R=-0.531). Finally, we observed significantly poorer prognosis in the lower LINE-1 methylation group (HR=2.8, P=0.015, compared to the higher methylation group). In conclusion, DNA methylation levels of repetitive elements, especially of LINE-1, are associated with the frequency of chromosomal deletions and prognosis in MM. 67 MM samples and 6 monoclonal gammopathy of undetermined significance (MGUS) samples were analyzed, all samples were selected by CD138 sorting
2012-03-01 | E-GEOD-33685 | biostudies-arrayexpress