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Genome wide mapping of histone acetyltransferase MOF binding in murine ES cells (sequencing)

ABSTRACT: We report the application of illumina sequencing technology for high-throughput profiling of histone acetyltransferase Mof in mouse embryonic stem cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells. We find that Mof widely binds to mouse genome and mark genes that are expressed, poised for expression, or stably repressed. Mof binds to both gene promoters and coding regions, exhibiting two modes of binding. This study provides a framework for understanding the function of Mof in regulating ESC core transcription network. Examination of Mof binding patterns in ES cells

ORGANISM(S): Mus musculus

SUBMITTER: Yali Dou

PROVIDER: E-GEOD-37268 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The histone acetyltransferase MOF is a key regulator of the embryonic stem cell core transcriptional network.

Li Xiangzhi X Li Li L Pandey Ruchi R Byun Jung S JS Gardner Kevin K Qin Zhaohui Z Dou Yali Y

Cell stem cell 20120801 2

Pluripotent embryonic stem cells (ESCs) maintain self-renewal and the potential for rapid response to differentiation cues. Both ESC features are subject to epigenetic regulation. Here we show that the histone acetyltransferase Mof plays an essential role in the maintenance of ESC self-renewal and pluripotency. ESCs with Mof deletion lose characteristic morphology, alkaline phosphatase (AP) staining, and differentiation potential. They also have aberrant expression of the core transcription fact ...[more]

PMID: 22862943

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Expression data from mouse ES cells after control RNAi (scramble siRNAs) or specific RNAi (siRNAs for specific genes) treatment

Project description:To address the functional role of MOF in mammalian X upregulation, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Mof mRNA. We found that MOF knockdown in mouse ES cells caused a greater drop in expression of X-linked genes compared to autosomal genes, as measured by expression array analyses. The strongest effect was observed on medium-expressed X-linked genes. We next examined components of the two known MOF protein complexes, MSL1 (male-specific lethal1) and NSL1 (nonspecific lethal1). Knockdown of MSL1 but not NSL1 in undifferentiated female ES cells PGK12.1 specifically caused a decrease in expression levels of X-linked genes. Cells co-transfected with both MOF and MSL1 siRNAs had similar expression changes to MSL1 knockdown alone, indicating that these components probably operate within the same complex but are not additive. Our findings that key components of the MSL but not NSL complex play a role in upregulation of mammalian X-linked genes in ES cells. Mouse ES cells were treated by Invitrogen scramble siRNA duplexes or specific siRNA duplexes and used for RNA extraction and hybridization on Affymetrix microarrays. Six RNA samples from two independent double-RNAi treatments and one single-RNAi treatment in undifferentiated female ES cells PGK12.1, and RNA samples from two single-RNAi treatments in undifferentiated male ES cells WD44 or E14 were assayed for expression changes by arrays. RNA samples from three MSL1RNAi treatments, two MOF/MSL1RNAi treatments and three NSL1RNAi treatments in undifferentiated female ES cells PGK12.1 were assayed by arrays.

2013-02-15 | E-GEOD-44252 | biostudies-arrayexpress

Upregulation of the mammalian X chromosome is associated with enhanced transcription initiation, MOF-mediated H4K16 acetylation, and longer RNA half-life

Project description:Many animal species employ a chromosome-based mechanism of sex determination, which has led to coordinate evolution of dosage compensation systems. Dosage compensation not only corrects the imbalance in the number of X-chromosomes between the sexes, but is also hypothesized to correct dosage imbalance within cells due to mono-allelic X expression and bi-allelic autosomal expression, by upregulating X-linked genes (termed M-bM-^@M-^XOhnoM-bM-^@M-^Ys hypothesisM-bM-^@M-^Y). To identify molecular mechanisms of X upregulation in mammals we established genome-wide profiles for the initiation and elongation forms of RNA polymerase II (PolII), PolII-S5p (phosphorylated at serine 5) and PolII-S2p (phosphorylated at serine 2), and for histone modifications in mouse cell lines and tissues. We found that in addition to being enriched in PolII-S5p but not in PolII-S2p, X-linked promoters were also enriched in two epigenetic marks, H4K16ac and H2AZ, dependent on expression levels. To address the function of the H4K16 acetyltransferase MOF occupancy profiles were established and knockdowns of MOF and MSL1 were done in mouse ES cells. Our results support a conserved role for the MSL complex to enhance transcription initiation of X-linked genes. Comparison of the profiles of RNA PolII, the H4K16ac acetyltransferase MOF and histone active marks on the X versus autosomes in mouse

2013-03-05 | E-GEOD-44835 | biostudies-arrayexpress

Identificaiton of novel acetylation sites in UHRF1 mediated by acetyltransferase MOF

Project description:The multi-domain protein UHRF1 (ubiquitin-like, containing PHD and RING finger domains, 1) recruits DNMT1 for DNA methylation maintenance during DNA replication. Here, we show that MOF (Males absent On the First) is an acetyltransferase of UHRF1 to acetylate UHRF1 at Lys670 in the pre-RING linker region whereas HDAC1 is a deacetylase of UHRF1 at the same site. The MOF/HDAC1-mediated acetylation in UHRF1 is cell-cycle regulated and peaks at G1/S phase, in line with the function of UHRF1 in recruiting DNMT1 to maintain DNA methylation. In addition, UHRF1 acetylation significantly enhances its E3 ligase activity and elimination of UHRF1 acetylation at these sites attenuates UHRF1-mediated H3 ubiquitination, which in turn impairs the DNMT1 recruitment and DNA methylation. Taken together, these findings not only identify MOF as a new acetyltransferase for UHRF1 but also reveal a novel mechanism underlying the regulation of DNA methylation maintenance through MOF-mediated UHRF1 acetylation.

2024-03-06 | PXD040426 | Pride

Genome wide mapping of histone acetyltransferase MOF binding in murine ES cells.

Project description:We report the application of Affy based microarray technology for profiling of gene expression in mouse embryonic stem cells with or without histone acetytransferase MOF. We find that Mof regulates a wide range of genes in mouse ESCs including those important for ESC pluripotency and ESC differentiation. Mof deletion leads to similar number of genes that are up or down regulated. This study provides a framework for understanding the function of Mof in regulating ESC core transcription network. Compare gene expression difference in two cell lines

2012-04-11 | E-GEOD-37109 | biostudies-arrayexpress

Tiling path and RNAi of Drosophila KO MSL1, MLS3, and MOF reveals MOF as a key regulator of dosage compensation and gene expression

Project description:Effect of MSL1, MSL3 and MOF RNAi KOs in Drosophila SL-2 and Kc cells.

2008-06-09 | E-MEXP-1505 | biostudies-arrayexpress

Comparative FAIRE-seq analysis reveals distinguishing features of the chromatin structure of ground state- and primed pluripotent cells

Project description:We utilized FAIRE-seq to identify accesible chromatin in mouse embryonic-, epiblast-, and neural- stem cells in addition to mouse embryonic fibroblasts. Analysis of these data sets reveal cell type specific chromatin signatures that differentiate naïve and primed pluripotency. Functional analysis of type-specific peaks revealed cell-type specific enhancers. FAIRE-seq of mESC, EpiSC, NSC and MEF

2015-01-01 | E-GEOD-58520 | biostudies-arrayexpress

Chromatin immunoprecipitation to determine MSL1, MSL3, MOF and H4K16Ac binding in Drosophila SL2 and Kc cells reveals MOF as a key regulator of dosage compensation and gene expression in Drosophila

Project description:Genome-wide binding profiles of MSL1, MSL3, MOF and H4K16Ac in Drosophila SL2 and Kc cells.

2008-06-12 | E-MEXP-1508 | biostudies-arrayexpress

ChIP-Seq analysis of ER binding sites in MCF7 breast cancer cells

Project description:Estrogen Receptor (ER) is a hormonal transcription factor that plays important roles in breast cancer. It functions primarily through binding to the regulatory regions of target genes containing the consensus ERE motifs. In order to identify ER target genes and re-define the ERE motifs we performed ChIP-Seq analysis of ER in MCF7 breast cancer cell line. Applying a novel computational algorithm named Hybrid Motif Sampler (HMS), specifically designed for TFBS motif discovery in ChIP-Seq data, we were able to detect an improved ERE motif and reveal intra-motif dependency especially in neighboring base pairs. MCF7 cells were grown in starving medium (RPMI with 5% FCS) for 3 days prior to the treatment with 10 nM β-estradiol or vehicle control for 45 minutes. ChIP was done using an anti-ER antibody in both the ethl-treated and the E2-treated cells. ChIP-Seq sample prep and sequencing were done following the manufacture's protocol using the Genome Analyzer (Illumina). The read files were analyzed using ethl-treated as control for E2-treated, leading to one final peak file.

2010-02-01 | E-GEOD-19013 | biostudies-arrayexpress

The MOF-containing NSL complex associates globally with housekeeping genes, but activates only a defined subset

Project description:This SuperSeries is composed of the following subset Series: GSE30989: MOF-containing NSL complex specifically binds promoters of most, but stimulates only a specific subset of, housekeeping genes (ChIP-chip dataset) GSE30990: MOF-containing NSL complex specifically binds promoters of most, but stimulates only a specific subset of, housekeeping genes (expression dataset) Refer to individual Series

2011-10-28 | E-GEOD-30991 | biostudies-arrayexpress

Enhancer bound proteome of intronic Ig Emu enhancer with E1 box mutation control bait

Project description:The specificity of humoral immune responses depends on the functional rearrangement and expression of only one allele of immunoglobulin (Ig) genes. Here, we analyzed the comprehensive proteome of the murine Ig Emu enhancer, which governs the rearrangement and expression of the Ig mu heavy chain allele. By mass spectrometry of proteins bound at wild type versus mutant Emu enhancers, we identified Emu-binding proteins and associated multi-protein complexes. We found that the MSL/MOF complex, a regulator of gene dosage compensation in flies, binds Emu via transcription factor YY1 and facilitates Emu-driven chromatin looping and promoter interaction. Msl2 gene knockout in primary pre-B cells or Mof heterozygosity in mice reduced mu gene expression. In this data set we compare proteins binding to the wild-type Emu versus a DNA bait control for which the E1 box of the core enhancer region was mutated (E1mt).The E1mt abrogates binding of proteins recognizing the E1 box (e.g. YY1). Max LFQ quantitative proteomics was employed in an approach incubating wild-type and control DNA with (unlabeled) nuclear extracts.

2024-10-25 | PXD045704 | Pride

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