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Top2Î² ChIP-chip

ABSTRACT: Chromatin IP was performed with Top2Î² antibodies in WT neurons and hybridized to custom designed tiling array. HD 2.1 (custom- made)

ORGANISM(S): Mus musculus

SUBMITTER: Dirk Schuebeler

PROVIDER: E-GEOD-27246 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Target genes of Topoisomerase IIβ regulate neuronal survival and are defined by their chromatin state.

Tiwari Vijay K VK Burger Lukas L Nikoletopoulou Vassiliki V Deogracias Ruben R Thakurela Sudhir S Wirbelauer Christiane C Kaut Johannes J Terranova Remi R Hoerner Leslie L Mielke Christian C Boege Fritz F Murr Rabih R Peters Antoine H F M AH Barde Yves-Alain YA Schübeler Dirk D

Proceedings of the National Academy of Sciences of the United States of America 20120402 16

Topoisomerases are essential for DNA replication in dividing cells, but their genomic targets and function in postmitotic cells remain poorly understood. Here we show that a switch in the expression from Topoisomerases IIα (Top2α) to IIβ (Top2β) occurs during neuronal differentiation in vitro and in vivo. Genome-scale location analysis in stem cell-derived postmitotic neurons reveals Top2β binding to chromosomal sites that are methylated at lysine 4 of histone H3, a feature of regulatory regions ...[more]

PMID: 22474351

Similar Datasets

Gene regulation and priming by Topoisomerase IIÎ± in embryonic stem cells [ChIP-chip]

Project description:Topoisomerases are essential for resolving topological problems in the genome, while their function in gene regulation, especially during cellular differentiation, remains elusive/unknown. We reveal that the expression of two Topo II isoforms, Top2Î± and Top2Î², is characteristic of dividing and postmitotic tissues, respectively. In embryonic stem cells, Top2Î± preferentially binds to promoters embedded in an active chromatin environment. Inhibition of Top2Î± activity results in misregulation of target gene expression that accompanies accumulation of double-strand breaks. Common targets of Top2Î± and Top2Î² are housekeeping genes while their unique targets are involved in proliferation/pluripotency and neurogenesis (Can we say this as this might be because we are driving neurons from ES cells), respectively. Moreover, a small subset of Top2Î± targets exhibit bivalent chromatin state that is resolved upon differentiation concomitant with their activation and occupancy by Top2Î², a feature further observed for large lengthlong genes. These findings suggest that Top2Î± not only contributes to stem cell transcriptome regulation but may also prime developmental genes for subsequent activation by Top2Î². Chromatin IP was performed with Top2Î± antibodies in WT ES cells and hybridized to custom designed tiling array.

2013-10-10 | E-GEOD-45890 | biostudies-arrayexpress

Topoisomerase IIbeta occupies H3K4 methylated sites and regulates neuronal survival via repression of the neurotrophin receptor p75

Project description:This SuperSeries is composed of the following subset Series: GSE27245: Expression data from Top2Î² KO cells as well ICRF-193 treatment of in vitro derived neurons and cortical glutamatergic neurons GSE27246: Top2Î² ChIP-chip Refer to individual Series

2012-05-01 | E-GEOD-27247 | biostudies-arrayexpress

Gene regulation and priming by Topoisomerase IIÎ± in embryonic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-10-10 | E-GEOD-46070 | biostudies-arrayexpress

Genomic prevalence of heterochromatic H3K9me2 and transcription do not discriminate pluripotent from terminally differentiated cells (ChIP-chip)

Project description:Cellular differentiation entails reprogramming of the transcriptome from a pluripotent to a unipotent fate. This process was suggested to coincide with a global increase of repressive heterochromatin, which results in a reduction of transcriptional plasticity and potential. Here we report the dynamics of the transcriptome and an abundant heterochromatic histone modification, dimethylation of histone H3 at lysine 9 (H3K9me2), during neuronal differentiation of embryonic stem cells. In contrast to the prevailing model, we find H3K9me2 to occupy over 50% of chromosomal regions already in stem cells. Marked are most genomic regions that are devoid of transcription and a subgroup of histone modifications. Importantly, no global increase occurs during differentiation, but discrete local changes of H3K9me2 particularly at genic regions can be detected. Mirroring the cell fate change many genes show altered expression upon differentiation. Quantitative sequencing of transcripts reveals however that the total number of active genes is equal between stem cells and several tested differentiated cell types. Together, these findings reveal high prevalence of a heterochromatic mark in stem cells and challenge the model of low abundance of epigenetic repression and resulting global transcription in stem cells. Instead cellular differentiation entails local rather than global changes in epigenetic repression and transcriptional activity. Our dataset comprises of 2 ChIP-seq samples using chromatin from embryonic stem (ES) cells and derived terminal neurons (TN) which was immunoprecipitated, using antibodies against H3K27me3 and H3K4me2. For the same cells we generated H3K9me2 ChIP-chip samples in biological replicates. For ES cells, neurons and mouse embryonic fibroblasts (MEFs) we generated biological replicates of RNA-seq data.

2011-06-21 | E-GEOD-27724 | biostudies-arrayexpress

Acetylation at the lateral surface of the nucleosome at lysine 64 of H3 regulates chromatin dynamics and defines transcriptionally active chromatin

Project description:Post-translational modifications of proteins have emerged as a major mechanism for regulating gene expression. Yet our understanding of how histone modifications directly affect chromatin function remains limited. Here, we investigate acetylation of histone H3 at lysine 64 (H3K64ac), a previously uncharacterized acetylation site on the lateral surface of the histone octamer. We show that H3K64ac regulates nucleosome dynamics by (i) destabilizing nucleosomes, and (ii) regulating chromatin remodelling. Both of these functions have the potential to regulate gene expression. In line with this, we show that the p300 co-activator acetylates H3K64 both in vitro and in vivo. H3K64ac is enriched at the transcriptional start sites (TSS) of active genes and defines transcriptionally active chromatin in ES cells. Moreover, we find that H3K64ac is dynamic during developmental reprogramming, and during mammalian spermatogenesis where H3K64 hyperacetylation precedes histone replacement. Consistent with a function in transcriptional activation, H3K64ac opposes its repressive counterpart H3K64me3. Our findings reveal an important role for a histone modification within the nucleosome core as a regulator of chromatin function in vivo and they demonstrate that lateral surface modifications can define functionally opposing chromatin states. In this study, 2 biological replicate samples for H3K64ac ChIP and one sample of H3K9ac ChIP in mouse emryonic stem cells were analyzed using custom designed Nimblegen HD2.1oligonucleotide tiling arrays.

2014-03-18 | E-GEOD-35355 | biostudies-arrayexpress

Genomic prevalence of heterochromatic H3K9me2 and transcription do not discriminate pluripotent from terminally differentiated cells (ChIP-seq)

2011-06-21 | E-GEOD-27827 | biostudies-arrayexpress

Methylated DNA Immunoprecipitation (MeDIP) using a custom type 2 diabetes and related phenotypes array

Project description:Custom array designed to tile Linkage Disequilibrium Blocks of T2D GWAS SNPs, monogenic candidates for T2D and Obesity, and all plausible imprinted loci from human and mouse data. Case Control comparison of MeDIP for Type 2 Diabetes. MeDIP versus Input fraction.

2010-12-01 | E-GEOD-20553 | biostudies-arrayexpress

Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

Project description:Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFÎ²-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. Ablation of Ezh2 expression prevents EMT, while forced expression of Ezh2 restores EMT in Sox4-deficient cells. Ezh2-mediated H3K27me3 marks associate with key EMT genes, representing an epigenetic EMT signature that predicts patient survival. Our results identify Sox4 as a master regulator of EMT by governing the expression of the epigenetic modifier Ezh2. Our Dataset comprises of 12 ChIP-seq samples using chromatin from NMuMG cells which was immunoprecipitated using H3K27me3-specific antibody during TGFÎ²-induced EMT (2ng/ml) at 6 different stages (day 0, 1, 4, 7, 10, 20).

2013-06-20 | E-GEOD-45579 | biostudies-arrayexpress

Chip-chip for H3K27me3 and H3K4me3 in DNA methylation deficient mouse embryonic fibroblasts

Project description:DNA methylation and the Polycomb Repression System are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear. By genome-wide mapping of the Polycomb Repressive Complex 2 (PRC2)-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and PRC2 from Polycomb-target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression. An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining PRC2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease. comparison of Dnmt1+/+ vs Dnmt1-/- mouse embryonic fibroblasts

2013-02-09 | E-GEOD-44149 | biostudies-arrayexpress

A chromatin-modifying function of JNK during stem cell differentiation

Project description:Signaling mediates cellular responses to extracellular stimuli. The c-Jun NH2-terminal kinase (JNK) pathway exemplifies one sub-group of Mitogen-activated protein (MAP) kinases, which besides established functions in stress response, also contributes to developmental processes by an unknown mechanism 1-4. Here we show by genome-wide location analysis that JNK binds directly to a large set of active promoters during differentiation of stem cells to neurons. Bound promoters are not enriched for the canonical AP?1 target sites yet for binding motifs for the transcription factor NF?Y. NF-Y indeed occupies these predicted sites genome-wide in vivo and overexpression of a dominant-negative form of NF?YA reduces JNK presence on chromatin. Histone H3 is a substrate for JNK kinase activity in vitro and JNK bound promoters are preferentially enriched for Histone H3 phosphorylated at Serine 10. Inhibition of JNK signaling in postmitotic neurons reduces this chromatin phosphorylation as well as expression of target genes. Together this establishes MAP kinase binding and function on chromatin at a novel class of target genes during stem cell differentiation. Our Dataset comprises 5 ChIP-seq samples using chromatin from ES, NP and TN cells which was immunoprecipitated, using antibodies against H3K27me3, H3K4me2, RNA Pol II, JNK1/3 and NF-YA. From the same cells we generated biological replicates of RNA-seq data.

2011-12-18 | E-GEOD-25532 | biostudies-arrayexpress

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