Microarray analyses for wild type and Mof knockout murine ES cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE37109 | GEO | 2012/04/12
SECONDARY ACCESSION(S): PRJNA158985
REPOSITORIES: GEO
Similar Datasets
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
Project description: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.
2012-08-09 | GSE37268 | GEO
Project description: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
2012-08-09 | E-GEOD-37268 | biostudies-arrayexpress
Project description:We assessed the genome-wide binding of the histone acetylase MOF and members of its two associated complexes, the male-specific lethal and the non-specific lethal complex (MSL, NSL). We generated ChIP-seq profiles for MOF, MSL1, MSL2, KANSL3, and MCRS1 from mouse embryonic stem cells and neuronal progenitor cells. By using two replicates per sample and stringent filtering criteria, we identify five basic groups of genome regions where the proteins show either mutual or exclusive binding. We find that the NSL complex members (KANSL3, MCRS1) target the TSSs of broadly expressed genes with housekeeping functions in both cell types. MOF and particularly the MSL complex target a subset of these NSL-complex-targets, too. In addition, we find several thousand TSS-distal binding sites, particularly in ESCs, where KANSL3, MSL2 and MCRS1 show strong enrichments for annotated ESC enhancers. The vast majority of the binding to these ESC distal regulatory elements is lost in NPCs. Finally, we identify mostly intronic and intergenic regions with predominant MSL2 enrichments without the presence of its known interactors. These binding sites do not overlap with ESC marks of active chromatin (e.g. DNase hypersensitivity sites), but the they increase in number upon differentiation and we detect a strong signature of the (CAGA)n motif. Our study provides the first comprehensive analysis of MOF in the context of its two complexes in the mouse and reveals shared as well as distinct and dynamic functions for gene regulation and pluripotency. ChIP-seq of MOF and members of its associated complexes (MSL complex: MSL1, MSL2; NSL complex: KANSL3, MCRS1) in male mouse embryonic stem cells and neuronal progenitor cells derived from them.
2014-06-03 | E-GEOD-51746 | biostudies-arrayexpress
Project description:We assessed the genome-wide binding of the histone acetylase MOF and members of its two associated complexes, the male-specific lethal and the non-specific lethal complex (MSL, NSL). We generated ChIP-seq profiles for MOF, MSL1, MSL2, KANSL3, and MCRS1 from mouse embryonic stem cells and neuronal progenitor cells. By using two replicates per sample and stringent filtering criteria, we identify five basic groups of genome regions where the proteins show either mutual or exclusive binding. We find that the NSL complex members (KANSL3, MCRS1) target the TSSs of broadly expressed genes with housekeeping functions in both cell types. MOF and particularly the MSL complex target a subset of these NSL-complex-targets, too. In addition, we find several thousand TSS-distal binding sites, particularly in ESCs, where KANSL3, MSL2 and MCRS1 show strong enrichments for annotated ESC enhancers. The vast majority of the binding to these ESC distal regulatory elements is lost in NPCs. Finally, we identify mostly intronic and intergenic regions with predominant MSL2 enrichments without the presence of its known interactors. These binding sites do not overlap with ESC marks of active chromatin (e.g. DNase hypersensitivity sites), but the they increase in number upon differentiation and we detect a strong signature of the (CAGA)n motif. Our study provides the first comprehensive analysis of MOF in the context of its two complexes in the mouse and reveals shared as well as distinct and dynamic functions for gene regulation and pluripotency.
2014-06-03 | GSE51746 | GEO
Project description:We have studied the regulatory potential of MYST1-(MOF)-containing MSL and NSL complexes in mouse embryonic stem cells (ESCs) and neuronal progenitors. We find that both complexes influence transcription by binding to promoters as well as TSS-distal enhancer regions. In contrast to flies, the MSL complex is not enriched on the X chromosome yet it is crucial for mammalian X chromosome regulation as it specifically regulates Tsix ncRNA, the major repressor of Xist lncRNA. MSL depletion leads to severely decreased Tsix expression, reduced REX1 recruitment, and consequently accumulation of Xist RNA in ESCs. The NSL complex provides additional, Tsix-independent repression of Xist by maintaining pluripotency. MSL and NSL complexes therefore act synergistically by using distinct pathways to ensure a fail-safe mechanism for the repression of X inactivation in ESCs. We have performed ChIP-seq of KANSL3, MCRS1, MOF, MSL1 and MSL2 in mouse ESCs, and KANSL3, MOF and MSL2 in NPCs, in duplicate and normalised against their inputs. We have also performed RNA-seq following knockdown of Kansl3, Mof, Msl1 and Msl2 mouse embryonic stem cells in triplicate. NB: Kansl3 and Mof knockdown-RNAseq are analyzed against their own scrambled controls, and Msl1 and Msl2 against another scrambled control triplicate.
2014-06-03 | E-GEOD-57698 | biostudies-arrayexpress
Project description:We have studied the regulatory potential of MYST1-(MOF)-containing MSL and NSL complexes in mouse embryonic stem cells (ESCs) and neuronal progenitors. We find that both complexes influence transcription by binding to promoters as well as TSS-distal enhancer regions. In contrast to flies, the MSL complex is not enriched on the X chromosome yet it is crucial for mammalian X chromosome regulation as it specifically regulates Tsix ncRNA, the major repressor of Xist lncRNA. MSL depletion leads to severely decreased Tsix expression, reduced REX1 recruitment, and consequently accumulation of Xist RNA in ESCs. The NSL complex provides additional, Tsix-independent repression of Xist by maintaining pluripotency. MSL and NSL complexes therefore act synergistically by using distinct pathways to ensure a fail-safe mechanism for the repression of X inactivation in ESCs.
2014-06-03 | GSE57698 | GEO
Project description:We report Illumina next generation RNA sequencing (RNAseq) of MLL-AF9 in vitro transformed murine LSKs upon genetic deletion of Mof. These gene expression data illustrate that Mof regulates the expression of genes involved in DNA damage response and chromatin stability in MLL-AF9 transformed cells.
2017-08-30 | GSE80671 | GEO
Project description:Purpose: Conditional MOF deletion in mouse livers resulted in acute hepatic necrosis. The goal of this study was to identify transcriptomic changes in the livers of MOF-depeleted mice livers compared to WT. Methods: Transcriptomic profiles of MOF∆ and WT mouse livers were generated in triplicate. Sequenced reads were quality filtered using Trimmomatic. Quality reads were aligned to the mouse genome using TopHat2. Reads were counted using htseq-count and differentially expressed transcripts were identified using DESeq. Results: 1408 differentially expressed genes were identified between MOF∆ and WT livers. 774 genes were down-regulated in MOF∆ and primarilly associated with metabolic pathways. Branched chain amino acid and fatty acid metabolic pathways, which are deregulated in non-alcoholic fattly liver disease (NAFLD) prgression were down-regulated. 664 genes were upregulated and associated with increased proliferation. Conclusions: These data show that MOF is required for maintaining proper metabolic function in the liver and deregulation of MOF may be involved in progression of NAFLD.
2018-01-31 | GSE106369 | GEO
Project description:Histone acetylation is sensitive to metabolic cues, however interplay between histone acetyl transferases and cellular metabolism remains poorly understood. Here we report the localization of a classical nuclear HAT- MOF and members of Non-Specific Lethal complex in mitochondria. MOF regulates expression of oxidative phosphorylation (OXPHOS) genes, residing in both nuclear and mitochondrial genomes, selectively in aerobically respiring cells. Furthermore, MOF/KANSL1 depletion causes impaired mitochondrial translation and reduced respiration. MOF loss is catastrophic for tissues with high-energy consumption. In mouse hearts, Mof knockout causes hypertrophic cardiomyopathy, compromised ventricular contractility/ stroke volume and ultimately leads to cardiac failure within three weeks of birth. RNA-seq analysis of the cardiomyocytes revealed deregulation of mitochondrial nutrient metabolism and OXPHOS pathways. Consistently, electron microscopy on affected tissues revealed mitochondrial deterioration with high tissue heterogeneity, commonly observed in mitochondrial diseases. Thus, we reveal a novel function of MOF in mitochondrial homeostasis and propose MOF as a sensor connecting epigenetic regulation to metabolism.
2016-10-21 | GSE77784 | GEO