ChIP-on-chip from acute myeloid leukemia cell lines and clinical samples for H3K4me3, H3K27me3, and EZH2
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE16730 | GEO | 2009/08/15
SECONDARY ACCESSION(S): PRJNA117419
REPOSITORIES: GEO
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Project description:Histone modifcations at the p15INK4b gene were compared in sample with p15INK4b DNA methylation vs. samples with no DNA methylation AML clinical samples without DNA methylation exhibit bivalent histone modifications at p15INK4b, while clinical samples with DNA methylation display lower H3K4me3 and retain H3K27me3 Comparison of AML cell lines and clinical samples with p15INK4b DNA methylation to those free of DNA methylation. AML cell lines KG-1, KG-1a Kasumi-1, AML-193 have p15INK4b DNA methylation. AML patient samples AML6, AML7, AML8 have p15INK4b DNA methylation.
2010-05-06 | E-GEOD-16730 | biostudies-arrayexpress
Project description:Multicellular organism requires concise gene regulation during ontogeny and epigenetic modifications, such as DNA methylation and histone modification, facilitate the concise regulation. The conservative reprogramming patterns of DNA methylation in vertebrates have been well described but knowledge of how histone modifications are passed on to zygote from gametes are limited and conservations of histone modifications are not clear.We profiled H3K4me3/H3K27me3 modifications in gametes and early embryos in zebrafish and find out that patterns in gene promoter regions have been largely set to either bivalent or active states in gametes and then passed on to zygote. Bivalent states are partially maintained and active states are restored to match sperm’s pattern. But repressive H3K27me3 modifications as well as stage specific modifications in promoter regions are discarded. Prior to zygotic genome activation, patterns of genes that initialize ZGA have been converted to non-repressive states to coordinate gene expression. Histone modification in hyper methylated promoter peaks are erased independent of DNA methylome reprogramming. Comparative analysis revealed that functions of bivalent and active genes passed on from gametes are conserved in vertebrates and gene age preferences by bivalent and active histone modifications are also confirmed in vertebrates.
2019-04-17 | GSE110663 | GEO
Project description:Aberrational epigenetic marks are believed to play a major role in establishing the abnormal features of cancer cells. Rational use and development of drugs aimed at epigenetic processes requires an understanding of the range, extent, and roles of epigenetic reprogramming in cancer cells. Using ChIP-chip and MeDIP-chip approaches, we localized well-established and prevalent epigenetic marks (H3K27me3, H3K4me3, H3K9me3, DNA methylation) on a genome scale in several lines of putative glioma stem cells (brain tumor stem cells, BTSCs) and, for comparison, normal human fetal neural stem cells (fNSCs). We determined a substantial M-bM-^@M-^\coreM-bM-^@M-^] set of promoters possessing each mark in every surveyed BTSC cell type, which largely overlapped the corresponding fNSC sets. However, there was substantial diversity among cell types in mark localization. We observed large differences among cell types in total number of H3K9me3+ positive promoters and peaks and in broad modification areas for H3K27me3 and, to a lesser extent, H3K9me3. We verified that a change in a broad modification (defined as >50 kb peak length) affected gene expression of CACNG7. We detected large numbers of bivalent promoters, but most bivalent promoters did not display direct overlap of contrasting epigenetic marks, but rather occupied nearby regions of the proximal promoter. There were significant differences in the sets of promoters bearing bivalent marks in the different cell types and few consistent differences between fNSCs and BTSCs. Overall, our M-bM-^@M-^\core setM-bM-^@M-^] data establishes sets of potential therapeutic targets, but the diversity in sets of sites and broad modifications among cell types underscores the need to carefully consider BTSC subtype variation in epigenetic therapy. Our results point toward substantial differences among cell types in the activity of the production/maintenance systems for H3K9me3 and for broad regions of modification (H3K27me3 or H3K9me3). Finally, the unexpected diversity in bivalent promoter sets among these multipotent cells indicates that bivalent promoters may play complex roles in the overall biology of these cells. These results provide key information for forming the basis for future rational drug therapy aimed at epigenetic processes in these cells. ChIP-chip and MeDIP-chip localization of histone modifications and DNA methylation in glioma stem cells and fetal neural stem cells comparison of 4 lines of brain tumor stem cells to each other and to normal fetal neural stem cells
2014-08-30 | E-GEOD-60806 | biostudies-arrayexpress
Project description:Background Thousands of mammalian promoters are defined by co-enrichment of the histone tail modifications H3K27me3 (repressive) and H3K4me3 (activating) and are thus termed bivalent. It was previously observed that bivalent genes in human ES cells (hESC) are frequent targets for hypermethylation in human cancers, and depletion of DNA methylation in mouse embryonic stem cells has a marked impact on H3K27me3 distribution at bivalent promoters. However, only a fraction of bivalent genes in stem cells are targets of hypermethylation in cancer, and it is currently unclear whether all bivalent promoters are equally sensitive to DNA hypomethylation and whether H3K4me3 levels play a role in the interplay between DNA methylation and H3K27me3. Results We report the sub-classification of bivalent promoters into two groups—promoters with a high H3K27me3:H3K4me3 (hiBiv) ratio or promoters with a low H3K27me3:H3K4me3 ratio (loBiv). HiBiv are enriched in canonical Polycomb components, show a higher degree of local intrachromosomal contacts and are highly sensitive to DNA hypomethylation in terms of H3K27me3 depletion from broad Polycomb domains. In contrast, loBiv promoters are enriched in non-canonical Polycomb components, show lower intrachromosomal contacts and are less sensitive to DNA hypomethylation at the same genomic resolution. Multiple systems reveal that hiBiv promoters are more depleted of Polycomb complexes than loBiv promoters following a reduction in DNA methylation, and we demonstrate that H3K27me3 re-accumulates at promoters when DNA methylation is restored. In human cancer, we show that hiBiv promoters lose H3K27me3 and are more susceptible to DNA hypermethylation than loBiv promoters. Conclusion We conclude that bivalency as a general term to describe mammalian promoters is an over-simplification and our sub-classification has revealed novel insights into the interplay between the largely antagonistic presence of DNA methylation and Polycomb systems at bivalent promoters. This approach redefines molecular pathologies underlying disease in which global DNA methylation is aberrant or where Polycomb mutations are present.
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Project description:Histone modifcations and CTCF binding at the c-myb locus were compared in cell lines with c-myb expressing, which are myeloblatic M1 cells and leukemia cells with virus integration, VS. M1 cells without c-myb expression induced by IL-6. Distribution of active histone marks at the c-myb gene and the upstream regions are associated with active c-myb transcription. The enrichment of all of these active histone marks decreased with differentiation-induced down-regulation of c-myb, but increased and spread in tumor cells. ChIP-on-chip from murine myeloid cell line M1 and virus-induced myeloid leukemia cell lines for H3K4me3, H3K9/14ac, H3K4me1, H3K27me3, H3K9me3 and CTCF
2012-09-01 | E-GEOD-34770 | biostudies-arrayexpress
Project description:Histone modifcations and CTCF binding at the c-myb locus were compared in cell lines with c-myb expressing, which are myeloblatic M1 cells and leukemia cells with virus integration, VS. M1 cells without c-myb expression induced by IL-6. Distribution of active histone marks at the c-myb gene and the upstream regions are associated with active c-myb transcription. The enrichment of all of these active histone marks decreased with differentiation-induced down-regulation of c-myb, but increased and spread in tumor cells.
2012-09-01 | GSE34770 | GEO
Project description:Aberrational epigenetic marks are believed to play a major role in establishing the abnormal features of cancer cells. Rational use and development of drugs aimed at epigenetic processes requires an understanding of the range, extent, and roles of epigenetic reprogramming in cancer cells. Using ChIP-chip and MeDIP-chip approaches, we localized well-established and prevalent epigenetic marks (H3K27me3, H3K4me3, H3K9me3, DNA methylation) on a genome scale in several lines of putative glioma stem cells (brain tumor stem cells, BTSCs) and, for comparison, normal human fetal neural stem cells (fNSCs). We determined a substantial “core” set of promoters possessing each mark in every surveyed BTSC cell type, which largely overlapped the corresponding fNSC sets. However, there was substantial diversity among cell types in mark localization. We observed large differences among cell types in total number of H3K9me3+ positive promoters and peaks and in broad modification areas for H3K27me3 and, to a lesser extent, H3K9me3. We verified that a change in a broad modification (defined as >50 kb peak length) affected gene expression of CACNG7. We detected large numbers of bivalent promoters, but most bivalent promoters did not display direct overlap of contrasting epigenetic marks, but rather occupied nearby regions of the proximal promoter. There were significant differences in the sets of promoters bearing bivalent marks in the different cell types and few consistent differences between fNSCs and BTSCs. Overall, our “core set” data establishes sets of potential therapeutic targets, but the diversity in sets of sites and broad modifications among cell types underscores the need to carefully consider BTSC subtype variation in epigenetic therapy. Our results point toward substantial differences among cell types in the activity of the production/maintenance systems for H3K9me3 and for broad regions of modification (H3K27me3 or H3K9me3). Finally, the unexpected diversity in bivalent promoter sets among these multipotent cells indicates that bivalent promoters may play complex roles in the overall biology of these cells. These results provide key information for forming the basis for future rational drug therapy aimed at epigenetic processes in these cells. ChIP-chip and MeDIP-chip localization of histone modifications and DNA methylation in glioma stem cells and fetal neural stem cells
2014-08-30 | GSE60806 | GEO
Project description:Widespread misregulation of histone modifcations occur in FXS, most notably increases in marks associated with active transcription.
2017-08-18 | GSE81911 | GEO
Project description:DNA methylation is essential to mammalian development, and dysregulation can cause serious pathological conditions. Key enzymes responsible for deposition and removal of DNA methylation are known, but how they cooperate to tightly regulate the methylation landscape remains a central question. Utilizing a knockin DNA methylation reporter, we performed a genome-wide CRISPR/Cas screen in human embryonic stem cells to discover DNA methylation regulators. The top screen hit was an uncharacterized gene QSER1, which proved to be a key guardian of bivalent promoters and poised enhancers of developmental genes, especially those residing in DNA methylation valleys (or canyons). We further demonstrate cooperation of QSER1 and TET1 through genetic and biochemical interactions to inhibit DNMT3-mediated de novo methylation and safeguard developmental programs.
2021-03-19 | GSE169207 | GEO
Project description:Embryonic stem cells (ESCs) maintain pluripotency through unique epigenetic states. When ESCs commit to a specific cell lineage, changes in histone modifications and DNA methylation accompany the transition to more specialized cell types. Investigating how epigenetic regulation maintains pluripotency is a critical component in order to generate the required cell types for future clinical application. Uhrf1 is a widely known hemi-methylated DNA binding protein, playing a role in heterochromatin formation alongside G9a, Trim28 and HDACs. In addition, it has been demonstrated that Uhrf1 functions to maintain DNA methylation through the recruitment of Dnmt1. Although Uhrf1 is not essential in ESC self-renewal, it still remains elusive how Uhrf1 regulates pluripotency. Here, we set out to elucidate the role of Uhrf1 in pluripotent stem cells. We found that Uhrf1 forms a complex with the active trithorax group of transcriptional regulators, in particular the Setd1a/COMPASS complex. Our data show that loss of Uhrf1 causes a dramatic reduction of bivalent histone marks, in particular those associated with neuroectoderm and mesoderm specification. Overall, our data demonstrate that Uhrf1 safeguards the balance between pluripotency and differentiation via the Setd1a/COMPASSS complex, through which Uhrf1 mediates bivalent histone modifications.
2018-05-02 | GSE113913 | GEO