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Genome-wide analyses of the DRB response of the histone H3 Lys36 methylation state, as well as Ash1l occupancy in mouse embryonic stem cells.

ABSTRACT: Using wild type and Ash1l ?SET mutant embryonic stem cells, against a prevalent notion, here we report di-,tri-methylation of histone H3 Lys36 occur independently of ongoing transcription. Ash1l ?SET mutant shows the impaired methylation levels in broad range of genome. Intriguingly, data implicate that a binding of retinoic acid receptor to a certain genomic region promotes installation of the tri-methylation in the retinoic acid receptor-associated gene independent of its ongoing transcription. Examination of 2 different histone modifications in 2 cell types in 2 different conditions. Examination of Ash1l occupancy in 2 different conditions.

ORGANISM(S): Mus musculus

SUBMITTER: Takaho Endo

PROVIDER: E-GEOD-48421 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Ash1l methylates Lys36 of histone H3 independently of transcriptional elongation to counteract polycomb silencing.

Miyazaki Hitomi H Higashimoto Ken K Yada Yukari Y Endo Takaho A TA Sharif Jafar J Komori Toshiharu T Matsuda Masashi M Koseki Yoko Y Nakayama Manabu M Soejima Hidenobu H Handa Hiroshi H Koseki Haruhiko H Hirose Susumu S Nishioka Kenichi K

PLoS genetics 20131107 11

Molecular mechanisms for the establishment of transcriptional memory are poorly understood. 5,6-dichloro-1-D-ribofuranosyl-benzimidazole (DRB) is a P-TEFb kinase inhibitor that artificially induces the poised RNA polymerase II (RNAPII), thereby manifesting intermediate steps for the establishment of transcriptional activation. Here, using genetics and DRB, we show that mammalian Absent, small, or homeotic discs 1-like (Ash1l), a member of the trithorax group proteins, methylates Lys36 of histone ...[more]

PMID: 24244179

Similar Datasets

Genome-wide analyses of the DRB response of the histone H3 Lys36 methylation state, as well as Ash1l occupancy in mouse embryonic stem cells.

Project description:Using wild type and Ash1l ∆SET mutant embryonic stem cells, against a prevalent notion, here we report di-,tri-methylation of histone H3 Lys36 occur independently of ongoing transcription. Ash1l ∆SET mutant shows the impaired methylation levels in broad range of genome. Intriguingly, data implicate that a binding of retinoic acid receptor to a certain genomic region promotes installation of the tri-methylation in the retinoic acid receptor-associated gene independent of its ongoing transcription.

2013-11-20 | GSE48421 | GEO

Gene expression analysis of Ash1l mutant mouse embryonic stem cells.

Project description:Using wild type and Ash1l deltaSET mutant embryonic stem cells, here we report differences of gene expression pattern under undifferentiated state and differentiated state. Interestingly, gene expression changes are frequently observed in a subset of gene group that is regulated by Polycomb group proteins. Examination of 2 cell types in 2 different conditions.

2013-11-20 | E-GEOD-48419 | biostudies-arrayexpress

Genome-wide profiles of RNA polymerase II (Pol 2) DNA occupancy and the histone modifications H3K4me3 and H3K36me3 around the circadian cycle

Project description:To understand the transcriptional basis of circadian rhythms in mouse liver, we generated genome-wide profiles of RNA polymerase II (Pol 2) DNA occupancy and the histone modifications H3K4me3 and H3K36me3 around the circadian cycle. We found that Pol 2 occupancy at promoters and in gene bodies cycle in synchrony, suggesting that Pol 2 recruitment at promoters underlies circadian gene transcription. On average, Pol 2 occupancy precedes mRNA accumulation by about three hours. Promoters of transcribed genes have tri-methylated H3K4 residues even at their trough activity times, and the tri-methylation levels increase in phase with Pol 2 loading. In contrast, the tri-methylation of H3K36 residues lags transcription by three hours with amplitudes that are markedly shallower, indicating that this mark is less dynamic on the circadian time scale. The comparison of Pol 2 occupancy and mRNA accumulation revealed that both transcriptional and post-transcriptional regulatory mechanisms can account for diurnal mRNA profiles. Additional processed data and visualization tools are available at http://cyclix.vital-it.ch/ Contributed by members of CycliX consortium (http://cyclix.vital-it.ch/) 28 samples examinded, 7 Polr2b, 7 H3K4me3, 7 H3k36me3, 7 input samples.

2012-12-06 | E-GEOD-35788 | biostudies-arrayexpress

PML regulates NF-ÎºB phosphorylation and transcriptional activity

Project description:The transcription factor NF-ÎºB is considered the master regulator of the immune response but also acts broadly to regulate gene expression that influences cell survival, proliferation and differentiation. Post-translational modification of NF-ÎºB, phosphorylation in particular, is essential for the transactivation activity of NF-ÎºB. Emerging evidence suggests that the regulation of NF-ÎºB in the nucleus is critical in controlling gene expression. Promyelocytic Leukemia (PML) is a nuclear protein that forms nuclear bodies (PML NBs), sub-nuclear structures that are associated with transcriptionally active genomic regions that have been implicated in multiple processes such as apoptosis, senescence and anti-viral responses. Chromosomal translocations leading to the expression of a PML-retinoic acid receptor-Î± (PML-RARÎ±) fusion protein are causative for acute promyelocytic leukemia (APL) characterised by a differentiation block at the promyelocytic state of myeloid development. Here we demonstrate that PML is required for phosphorylation of NF-ÎºB p65 and that PML is essential for NF-ÎºB- induced transcriptional responses. Our analysis of available transcriptional profiles of all-trans retinoic acid treated acute promyelocytic leukemia (APL) cells identifies a NF-ÎºB transcriptional programme suppressed by PML-RARÎ±. We further demonstrate that PML-RARÎ± inhibits NF-ÎºB phosphorylation and transcriptional activity. Our findings demonstrate a critical role for PML in promoting NF-ÎºB transcriptional activity which may contribute to APL initiation and maintenance. WT and PML-/- MEFs were analysed for gene expression analysis. Total of 12 samples, inlcluding triplicates were utilized. WT MEFs and PML-/- were stimulated with TNFÎ± for three hours and analysed for gene expresison using unstimulated WT MEFs as control.

2016-06-01 | E-GEOD-47828 | biostudies-arrayexpress

Transcriptome analysis of auditory cortex in 1-month-old and 1-year-old Ash1l heterozygous mice with their age-matched WT littermates

Project description:Ash1l encodes a histone methyltransferase, a member of the trithorax group proteins, which regulates developmental essential gene expression by catalyzing H3K36 methylation and counteracting polycomb silencing. Accumulating reports suggest the loss-of-function mutants in Ash1l gene are associated with intellectual disability (ID), attention-deficit/hyperactivity (ADHD), autism spectrum disorder (ASD), Tourette syndrome (TS) and multiple congenital anomalies (MCA). We performed transcriptome analysis of auditory cortex in 1-month-old and 1-year-old Ash1l Ash1l heterozygous mice with their age-matched WT littermates via RNA sequencing (RNA-seq). Ash1l haploinsufficiency induces transcription alternation of genes involved in synaptic function and cortical development, implicating the deficits in synapse pruning and behavior in adult mice.

2022-01-25 | GSE184375 | GEO

Transcriptional profiling of dorsal striatum in 1-year-old WT mice and Ash1l heterozygous mice

Project description:Ash1l encodes a histone methyltransferase, a member of the trithorax group proteins, which regulates developmental essential gene expression by catalyzing H3K36 methylation and counteracting polycomb silencing. Accumulating reports suggest the loss-of-function mutants in Ash1l gene are associated with intellectual disability (ID), attention-deficit/hyperactivity (ADHD), autism spectrum disorder (ASD), Tourette syndrome (TS) and multiple congenital anomalies (MCA). We performed transcriptional profiling of dorsal striatum in 1-year-old Ash1l mutant brain via RNA sequencing (RNA-seq). Ash1l haploinsufficiency induces transcription alternation of genes involved in synaptic function and cortical development, implicating the deficits in synapse pruning and behavior in adult mice.

2022-01-25 | GSE173502 | GEO

Dynamic loss of H2B ubiquitylation without corresponding changes in H3K4 tri-methylation during myogenic differentiation

Project description:Ubiquitylation of H2B on lysine 120 (H2Bub) is associated with active transcriptional elongation. H2Bub has been implicated in histone cross-talk and is generally regarded to be a prerequisite for H3K4 and H3K79 tri-methylation in both yeast and mammalian cells. We performed a genome-wide analysis of epigenetic marks during muscle differentiation, and, strikingly, we observed a near-complete loss of H2Bub in the differentiated state. We examined the basis for global loss of this mark and found that the H2B ubiquitin E3 ligase, RNF20, was depleted from chromatin in differentiated myotubes, indicating that recruitment of this protein to genes substantially decreases upon differentiation. Remarkably, during the course of myogenic differentiation, we observed retention and acquisition of H3K4 tri-methylation on a large number of genes in the absence of detectable H2Bub. The Set1 H3K4 trimethylase complex was efficiently recruited to a subset of genes in myotubes in the absence of detectable H2Bub, accounting in part for H3K4 tri-methylation in myotubes. Our studies suggest that H3K4me3 deposition in the absence of detectable H2Bub in myotubes is mediated via Set1 and, perhaps, MLL complexes, whose recruitment does not require H2Bub. Thus, muscle cells represent a novel setting in which to explore mechanisms that regulate histone cross-talk. Mapping of H2Bub in growing myoblasts (MB) and fully differentiated myotubes (MT).

2012-03-06 | E-GEOD-34960 | biostudies-arrayexpress

Mll2 branch of the COMPASS family regulates bivalent promoters in mouse embryonic stem cells

Project description:Promoters of many developmentally regulated genes, in the embryonic stem cell state, have a bivalent mark of H3K27me3 and H3K4me3, proposed to confer precise temporal activation upon differentiation. Although Polycomb repressive complex 2 is known to implement H3K27 trimethylation, the COMPASS family member responsible for H3K4me3 at bivalently marked promoters was previously unknown. Here, we identify Mll2 (KMT2b) as the enzyme catalyzing H3K4 trimethylation at bivalently marked promoters in embryonic stem cells. Although H3K4me3 at bivalent genes is proposed to prime future activation, we detected no substantial defect in rapid transcriptional induction after retinoic acid treatment in Mll2-depleted cells. Our identification of the Mll2 complex as the COMPASS family member responsible for H3K4me3 marking at bivalent promoters provides an opportunity to reevaluate and experimentally test models for the function of bivalency in the embryonic stem cell state and in differentiation. ChIP-Seq in mouse embryonic stem (mES) cells for MLL2. ChIP-seq of H3K4me1, H3K4me3 and H3K27me3 for mES cells with RNAi against MLL2(shMLL2) and control (shGFP). ChIP-seq of H3K4me3 in mES cells with RNAi against MLL3 (shMLL3). RNA-seq of mES cells with RNAi against MLL2 and control (shGFP). RNA-seq of control mES cells (shGFP) or MLL2 RNAi mES cells (shMLL2) induced with RA for 6h and 12h.

2013-08-11 | E-GEOD-48172 | biostudies-arrayexpress

An Ezh2 and Ezh1 dual inhibitor, UNC1999, re-shapes the landscape of H3K27me3 versus H3K27ac in MLL-AF9-transformed murine leukemia

Project description:Ezh2 and EZH1 are histone H3 lysine 27 (H3K27)-specific methyltransferases. Their hyperactive mutations and overexpression were found in cancer including various hematological malignancies. UNC1999 is a highly selective inhibitor for both enzymes. It suppresses H3K27 tri- and di-methylation globally and inhibits growth of MLL-rearranged acute leukemia. Here we performed ChIP-Seq to profile how UNC1999 affects distribution of H3K27me3 and its antagonizing H3K27ac in MLL-AF9-immortalized leukemia cells. We also performed ChIP-seq of SUZ12, an essential common cofactor of EZH2 and EZH1 following compound treatments. We treated MLL-AF9 transformed murine leukemia cells with DMSO, UNC1999 or UNC2400 (an inactive analog compound of UNC1999). Cells were then collected and used for ChIP-Sequencing of Input, H3K27me3, SUZ12, and H3K27ac.

2014-10-30 | E-GEOD-62437 | biostudies-arrayexpress

Histone H3K36me2-specific methyltransferase ASH1L promotes the MLL-AF9-induced leukemogenesis

Project description:ASH1L and MLL1 are two histone methyltransferases that facilitate transcriptional activation during normal development. However, the roles of ASH1L and its enzymatic activity in the development of MLL-rearranged leukemias are not fully elucidated in Ash1L gene knockout animal models. In this study, we used an Ash1L conditional knockout mouse model to show that loss of ASH1L in hematopoietic progenitor cells impaired the initiation of MLL-AF9-induced leukemic transformation in vitro. Furthermore, genetic deletion of ASH1L in the MLL-AF9-transformed cells impaired the maintenance of leukemic cells in vitro and largely blocked the leukemia progression in vivo. Importantly, the loss of ASH1L function in the Ash1L-deleted cells could be rescued by wild-type but not the catalytic-dead mutant ASH1L, suggesting the enzymatic activity of ASH1L was required for its function in promoting MLL-AF9-induced leukemic transformation. At the molecular level, ASH1L enhanced the MLL-AF9 target gene expression by directly binding to the gene promoters and modifying the local histone H3K36me2 levels. Thus, our study revealed the critical functions of ASH1L in promoting the MLL-AF9-induced leukemogenesis, which provides a molecular basis for targeting ASH1L and its enzymatic activity to treat MLL-arranged leukemias.

2021-09-07 | GSE183413 | GEO

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