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Analysis of H3K79 methylation during reprogramming

ABSTRACT: Chromatin immunoprecipitation followed by Solexa sequencing for H3K27me3 and H3K79me2 in Fibroblasts, Embryonic stem cells, and fibroblast undergoing reprogramming Inhibition of the histone 3 lysine 79 (H3K79) methyltransferase increases repgoramming efficiency and genome-wide analysis of H3K79me2 distribution revealed that fibroblast-specific genes associated with the epithelial to mesenchymal transition lose H3K79me2 in the initial phases of reprogramming. Dot1L inhibition facilitates the loss of this mark from genes that are fated to be repressed in the pluripotent state.

ORGANISM(S): Homo sapiens

SUBMITTER: Amit Sinha

PROVIDER: E-GEOD-35791 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells

Project description:H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells Examination of H3K79me2 modifications between Lgr5(hi) stem cells and differentiated villus cells

2012-10-13 | E-GEOD-41542 | biostudies-arrayexpress

H3K79 methylation - cell cycle

Project description:Mammalian DNA replication starts at distinct chromosomal sites in a tissue-specific pattern coordinated with transcription, but previous studies have not yet identified a chromatin modification that correlates with the initiation of DNA replication. This submission is associated with a paper in which we report that replication initiation events are associated with a high frequency of methylation of histone H3 on lysine K79 (H3K79Me2 and H3K79Me3). H3K79Me2-containing chromatin exhibited the highest enrichment of replication initiation events observed in a single chromatin modification. Importantly, H3K79 methylation was enriched in chromatin containing a replicator (a DNA sequence capable of initiating DNA replication), but not in chromatin containing a mutant replicator that could not initiate replication. The association of H3K79Me2 with replication initiation sites was independent and not synergistic with other chromatin modifications. H3K79 methylation exhibited a wider distribution and greater abundance during S-phase, but regions of chromatin that were only modified during S-phase were not enriched in replication initiation events. In addition, the paper shows that depletion of DOT1L, the sole enzyme responsible for H3K79 methylation, triggered limited genomic over-replication. These data are consistent with the hypothesis that methylation of H3K79 associates with replication origins and marks replicated chromatin during S-phase to prevent re-replication and preserve genomic stability. Evaluation of HeK79 methylation in chromatin samples from cell cycle fractionated K562 leukemia cells. Unsyncrhonized untreated cultures of K562 cells were fractionated by size using centrifugal elutriation. Chromatin was isolated and subject to ChIP-Seq with antibodies directed against dimethylated and trimethylated lysine on histone H3.

2013-06-06 | E-GEOD-35294 | biostudies-arrayexpress

Analysis of H3K79 methylation during reprogramming

Project description:Chromatin immunoprecipitation followed by Solexa sequencing for H3K27me3 and H3K79me2 in Fibroblasts, Embryonic stem cells, and fibroblast undergoing reprogramming

2012-02-22 | GSE35791 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse ChIP-seq]

Project description:Purpose: To characterize the genome-wide distribution of H3K79me2 in murine MN1 driven myeloid leukemia Methods: We performed Chip-seq for the H3K79me2 in leukemias isolated from moribund mice that had been injected with common myeloid progenitors (CMPs) transduced with MSCV-MN1-GFP Results: H3K79me2 is enriched at key loci that 1. are bound by MN1 in the data set of Heuser et al, (Cancer Cell. 2011 Jul 12;20(1):39-52.), 2. upregulated upon transduction with MN1, and lose expression upon deletion of the H3K79 methyltransferase Dot1l. Conclusions: A leukemogenic program in MN1 leukemias is marked by H3K79me2 and dependent on this mark ChIP-Seq for H3K79me2 using MN1 driven leukemias isolated from the bone marrow of moribund mice.

2016-01-12 | E-GEOD-76746 | biostudies-arrayexpress

Epigenetic profiling of hematopoietic stem cells and leukemia stem cells

Project description:The histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations that involve the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in a murine MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3 and H3K36me3. Histone methylation patterns are highly abnormal on MLL-AF9 fusion target loci, defining a distinct epigenetic lesion involving H3K79. Conditional inactivation of Dot1l leads to specific down-regulation of direct MLL-AF9 targets and an MLL-translocation associated gene expression signature, while global transcription levels remain largely unaffected. This correlated with a greater sensitivity of leukemic blasts towards loss of Dot1l compared to normal hematopoietic cells. Development of in vivo leukemia was absolutely dependent on Dot1l. Chromatin immunoprecipitation followed by Solexa sequencing for H3K4me3, H3K27me3, H3K36me3, H3K79me2 and biotinylated MLL-AF9 in HSC, GMP and LSC.

2011-09-13 | E-GEOD-29130 | biostudies-arrayexpress

Degree of Recruitment of DOT1L to MLL-AF9 Defines Level of H3K79 Di- and Tri-methylation on Target Genes and Transformation Potential

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2015-04-30 | E-GEOD-64365 | biostudies-arrayexpress

Global epigenomic analysis of primary human pancreatic islets provides insights into type 2 diabetes susceptibility loci

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2010-11-02 | E-GEOD-23784 | biostudies-arrayexpress

Nucleosome positioning in the IMR90 cell line

Project description:Micrococcal nuclease (Mnase) treatment and sequencing of mononucleosomal DNA One single sample in the IMR90 fibroblast cell line

2015-03-03 | E-GEOD-44985 | biostudies-arrayexpress

Reprogramming of Human Fibroblasts into Hematopoietic Progenitors by Fusion With Human Fetal Liver CD34+ Cells (GenomeWideSNP_6)

Project description:Reprogramming of the human fibroblast genome into the state of the hematopoietic progenitors Two samples analyzed.

2011-08-03 | E-GEOD-23414 | biostudies-arrayexpress

ChIP-Seq of Histone Methylation and RNAP2 in Human Jurkat cells.

Project description:Three transcriptional states can be defined by histone modifications and RNA polymerase II enriched at promoters and across the body of genes. To gain insight into the active, poised and silent genes in human T-ALL cells, two antibodies against RNAP2, and antibodies against H3K4me3, H3K79me2, and H3K27me3 were used for chromatin immunoprecipitation coupled with massive parallel sequencing (ChIP-seq). Genomic DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against RNAP2, H3K4me3, H3K79me2, and H3K27me3 using whole cell extract (WCE) as a background control. ChIP was performed using a two antibody against hypophosphorylated forms of RNAP2 in two biological replicates. All other ChIPs were done in biological replicates with a single lane of sequencing.

2010-07-24 | E-GEOD-23080 | biostudies-arrayexpress

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