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Comparing genome-wide H3K36me3 levels in WT vs. dKDM4A mutant

ABSTRACT: dKDM4A is a Drosophila H3 K9/K36 me2/me3 demethylase, which has been disrupted here by P-element insertion. We compare whole-genome ChIP-chip in mutant and WT to look for target genes of dKDM4A.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE37016 | GEO | 2012/07/10

SECONDARY ACCESSION(S): PRJNA157523

REPOSITORIES: GEO

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Comparing genome-wide H3K36me3 levels in WT vs. dKDM4A mutant

Project description:dKDM4A is a Drosophila H3 K9/K36 me2/me3 demethylase, which has been disrupted here by P-element insertion. We compare whole-genome ChIP-chip in mutant and WT to look for target genes of dKDM4A. Two samples, WT and dkDM4A mutant. 2 biological replicates each. 2 arrays.

2012-07-09 | E-GEOD-37016 | biostudies-arrayexpress

H3K9me3 and H3K36me3 ChIP-seq in WT and H3.3 G34R mouse ES cells

Project description:Sequencing of paediatric gliomas has identified two common substitution mutations (K27M and G34R) in genes encoding histone H3.3. We introduced a single-copy H3.3 G34R targeted mutation in mouse ES cells and observed gains in H3K36me3 and H3K9me3 across the genome. Altered chromatin profiles correlated with enrichment of KDM4 A/B/C, a histone lysine (K9/K36) demethylase. RNA-seq of H3.3 G34R mutant showed disrupted gene expression patterns which also correlated with KDM4 enrichment. Expression of a single copy of H3.3 G34R at endogenous levels was sufficient to genocopy KDM4 triple-KO cells as determined by ChIP-seq and RNA-seq.

2018-07-08 | GSE106203 | GEO

Genomic deletion of malic enzyme 2 confers collateral lethality in pancreas cancer

Project description:Comparison of malic enzyme 3 (ME3) depleted vs non-depleted xenograft tumors. ME3 is an isoform of ME2.

2017-08-22 | GSE80411 | GEO

RNA-seq in WT and H3.3 G34R mouse ES cells

2018-07-08 | GSE106204 | GEO

Histone Demethylase Lsd1 is Required to Repress Hematopoietic Stem and Progenitor Cell Signatures During Blood Cell Maturation

Project description:Here we describe that lysine-specific demethylase 1 (Lsd1/KDM1a), which demethylates histone H3 on LysM-bM-^@M-^I4 or LysM-bM-^@M-^I9 (H3K4/K9), is an indispensible epigenetic governor of hematopoietic differentiation. Integrative genomic analysis in primary hematopoietic cells, combining global occupancy of Lsd1, genome-wide analysis of its histone substrates H3K4 mono- and di-methylation and gene expression profiling, reveals that Lsd1 represses hematopoietic stem and progenitor cell (HSPC) gene expression programs during hematopoietic differentiation. We found that Lsd1 function was not restricted to transcription start sites, but is also critical at enhancers. Loss of Lsd1 at these sites was associated with increased H3K4me1 and H3K4me2 methylation levels on HSPC genes and their derepression. Failure to fully silence HSPC genes compromised differentiation of hematopoietic stem cells and mature blood cell lineages. Our data indicate that Lsd1-mediated concurrent repression of enhancer and promoter activity of stem and progenitor cell genes is a pivotal epigenetic mechanism required for proper hematopoietic maturation. To identify direct target genes of Lsd1 in myeloid cells we mapped global occupancy of Lsd1 in 32D granuolocytic progenitor cells and compared H3K4me1/me2/me3 and H3K27ac histone modifications in Lsd1fl/fl (wild type) vs. Lsd1fl/f Mx1Cre (knockout) Gr1dim Mac1 granuolocytic progenitor cells.

2013-06-25 | E-GEOD-40440 | biostudies-arrayexpress

ChIP-seq of H3K4me1, me2 and me3 on mouse salivary gland cancer cells cultured in either adherent or non-adherent conditions

Project description:Investigating how the Wnt-driven Mll1 epigenome regulates salivary gland and head and neck cancer. We performed mRNA-seq and ChIP-seq of H3K4me1, me2 and me3 on mouse salivary gland cancer cells that are kept in two different growth conditions, adherent culture and non-adherent sphere culture. Mouse salivary gland cancer cells were isolated from salivary gland of transgenic mouse that harbor K14-Cre-induced Wnt/β-catenin gain-of-function and Bmpr1a loss-of-function mutations. Anti-H3K4me1 (C15410194), -me2 (C15410035) and -me3 (C15410003-50) antibodies were purchased from Diagenode. ChIP-seq was performed according to the protocols provided by Diagenode using the iDeal ChIP-seq kit for histones and the iDeal library preparation kit. For mRNA-seq, mRNA was extracted according to the standard TRIzol protocol (Invitrogen) and subjected to library preparation using the TruSeq stranded mRNA library preparation kit. Sequencing was performed with the TruSeq SBS Kit v3-HS (2 X 200 cycles) on an Illumina HiSeq 2000 sequencer.

2018-12-24 | E-MTAB-7514 | biostudies-arrayexpress

Genome wide mapping of histone 3 lysine 79 mono, di and trimethylation and histone 3 lysine 27 trimethylation in LSKs, GMPs and retroviral MLL-AF9 driven murine leukemias

Project description:We report the genome wide distribution of the three states of H3K79 methylation (H3K79me1/me2/me3) and H3K27me3 in mouse lineage negative Sca-1 positive Kit positive cells (LSKs), granulocyte macrophage progenitors (GMPs) and LSK derived MLL-AF9 leukemias in the presence or absence of the Af10 OM-LZ domain. Legend- MIT:MSCV-IRES-tdTomato (Empty vector control) and CRE (MIT vector with the Cre recombinase). We examined the H3K79 me1,me2,me3 and H3K27me3 profiles by ChIP-seq in lineage negative Sca-1 positive, Kit positive (LSK) cells, granulocyte macrophage progenitors (GMPs) and bone marrow cells from sacrificed terminally ill secondary MLL-AF9 positive leukemic mice. In case of the MLL-AF9 leukemias, the ChIP-seq experiments were performed in 2 conditions in the presence or absence of the Dot1l interacing octapeptide-motif leucine zipper (OM-LZ) domain of Af10. For the leukemia experiments, leukemias derived from the Af10 OM-LZ homozygous floxed background were transduced with MSCV-IRES-tdTomato control vector (MIT) or its Cre-recombinase expressing counterparts (CRE). Subsequently, we sorted tdTomato positive cells and injected them into sub-lethally irradiated syngenic secondary recipient mice. Seconday leukemias obtained from these MIT or CRE expressing cells were used for ChIP -seq studies.

2014-09-08 | E-GEOD-55038 | biostudies-arrayexpress

mRNA-seq of mouse salivary gland cancer cells cultured in adherent or non-adherent culture

Project description:Aim: investigate how the Wnt-driven Mll1 epigenome regulates salivary gland and head and neck cancer. We performed mRNA-seq and ChIP-seq of H3K4me1, me2 and me3 on mouse salivary gland cancer cells that are kept in two different growth conditions, adherent culture and non-adherent sphere culture. Mouse salivary gland cancer cells were isolated from salivary gland of transgenic mouse that harbor K14-Cre-induced Wnt/β-catenin gain-of-function and Bmpr1a loss-of-function mutations.

2018-12-24 | E-MTAB-7509 | biostudies-arrayexpress

Histone lysine-to-methionine mutation reprograms the histone methylation landscape and contributes to pleiotropic development in Arabidopsis

Project description:This study investigated the effect of expressing transgenic H3 with K36M missense mutations. We uncovered pleiotropic phenotypic defects and a strong loss of endogenous H3K36 methylation in all forms (me1,me2,me3)

2017-06-16 | GSE92449 | GEO

Dynamics of de novo heterochromatin assembly and disassembly at replication forks ensures fork stability

Project description:Chromatin is dynamically reorganized when DNA replication forks are challenged. However, the process of epigenetic reorganization and its implication for fork stability is poorly understood. Here, we discover a checkpoint regulated cascade of chromatin signaling that activates 5 the histone methyltransferase EHMT2/G9a to catalyze heterochromatin assembly at stressed replication forks. Using biochemical and single molecule chromatin fiber approaches, we show that G9a together with SUV39h1 induces chromatin compaction by accumulating the repressive modifications, H3K9me1/me2/me3, in the vicinity of stressed replication forks. This closed conformation is also favored by the G9a-dependent exclusion of the H3K9-demethylase 10 JMJD1A/KDM3A, which facilitates heterochromatin disassembly upon fork restart. Untimely heterochromatin disassembly from stressed forks by KDM3A enables PRIMPOL access, triggering ssDNA gap formation and sensitizing cells towards chemotherapeutic drugs. These findings may help explaining chemotherapy resistance and poor prognosis observed in cancer patients displaying elevated level of G9a/H3K9me3.

2023-05-12 | PXD041742 | Pride

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