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Histone genes transcription regulators binding in human cancer (U2OS) and normal (hTERT-RPE1) cells

ABSTRACT: The regulation of replication-dependent histone genes by CASP8AP2 and NPAT is likely direct, based on ChIP-seq. CASP8AP2 and NPAT ChIP-Seq peaks were enriched near transcription start sites (TSSs) of replication-dependent, but not replication-independent histone genes on chromosomes 1, 6 and 12 in both cell lines. HINFP ChIP-Seq peaks were enriched near transcription start sites (TSSs) of replication-dependent histone genes H4 and H2B and replication-independent histone genes H1FX and H1F0 in both cell lines. Another histone gene regulator, E2F1 also bound to TSSs of many histone genes mainly replication-independent.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69147 | GEO | 2016/09/01

SECONDARY ACCESSION(S): PRJNA284642

REPOSITORIES: GEO

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Histone genes transcription regulators binding in human cancer (U2OS) and normal (hTERT-RPE1) cells

Project description:The regulation of replication-dependent histone genes by CASP8AP2 and NPAT is likely direct, based on ChIP-seq. CASP8AP2 and NPAT ChIP-Seq peaks were enriched near transcription start sites (TSSs) of replication-dependent, but not replication-independent histone genes on chromosomes 1, 6 and 12 in both cell lines. HINFP ChIP-Seq peaks were enriched near transcription start sites (TSSs) of replication-dependent histone genes H4 and H2B and replication-independent histone genes H1FX and H1F0 in both cell lines. Another histone gene regulator, E2F1 also bound to TSSs of many histone genes mainly replication-independent. Examination of histone genes transcroption regulators binding by ChIP-seq in normal and cancer cell lines

2016-09-01 | E-GEOD-69147 | biostudies-arrayexpress

Differential response of normal and tumor cells to nucleosome depletion

Project description:Gene-expression in siRNA treated U2OS and hTERT-RPE1 cells showed that CASP8AP2, NPAT and HINFP do not regulate expression of each other, and do not have any common target genes, except histones. Most histone genes are downregulated in U2OS cells following loss of CASP8AP2, NPAT or HINFP. In normal cells, highly-expressed histone genes were downregulated, albeit less than in tumor cells following loss of CASP8AP2. The p53 target genes were upregulated relatively late, clearly after the changes in expression of histone genes were observed. U2OS and hTERT-RPE1 cells were treated with CASP8AP2, NPAT, HINFP or control siRNA in duplicates or triplicates and collected for RNA purification on 1st, 2nd and 3d days.

2016-09-01 | E-GEOD-69148 | biostudies-arrayexpress

Differential response of normal and tumor cells to nucleosome depletion

2016-09-01 | GSE69148 | GEO

H3K4me3 modification profiling of Huntingtons disease and control human post-mortem prefrontal cortex brain samples

Project description:Huntingtonâs disease (HD) is an autosomal-dominant neurodegenerative disorder resulting from expansion in the number of CAG repeats in the coding region of exon 1 of the Huntingtin (HTT) gene. One of the most widely studied chromatin modifications is trimethylated lysine 4 of histone 3 (H3K4me3). Here, we conducted the first comprehensive study of H3K4me3 ChIP-sequencing in neuronal chromatin from the prefrontal cortex of six HD cases and six non-neurologic controls. We examined two classes of H3K4me3 peaks; those located near transcription start sites (TSSs) (termed âproximalâ) and those located distantly from TSSs (termed âdistalâ). We detected 2,830 differentially enriched H3K4me3 peaks between HD and controls, with 55% of them down regulated in HD. We found an unexpected discordance between levels of H3K4me3 and mRNA, with H3K4me3 predominantly reduced in HD and mRNA predominantly increased in HD. Gene ontology (GO) term enrichment analysis of the genes associated with the proximally positioned peaks, revealed diverse biological process terms with organ morphogenesis and positive regulation of gene expression most frequently implicated. GO terms relating to transcription and the extracellular matrix were also observed. Approximately 36% of the distal peaks co-localized to enhancer sites, with six transcription factors and chromatin remodelers differentially enriched in HD H3K4me3 distal peaks, including EZH2 and SUZ12, two core subunits of the polycomb repressive complex 2 (PRC2). Moreover, sequences repressed by polycomb in normal frontal cortex were significantly depleted in HD-enriched peaks, suggesting that H3K4me3 histone hypermethylation is linked to dysregulated polycomb activity in the HD neuronal epigenome. 12 H3K4me3 ChIP-seq libraries (6 Huntington's disease, 6 neurologically normal control), and 1 input DNA library (neurologically normal control)

2015-12-14 | E-GEOD-68952 | biostudies-arrayexpress

Histone acetyltransferase 2 links H4 acetylation, H2A.Z deposition and transcription start site-choice in African trypanosomes

Project description:Both, acetylation of histones and of histone variant H2A.Z are conserved features of eukaryotic transcription start sites (TSSs) and both features appear to be critical for correct transcription initiation. However, complex patterns of transcriptional regulation have complicated the establishment of functional links between histone acetylation, H2A.Z deposition and their importance in transcription regulation. To elucidate these links, we took advantage of the unusual genome organization in Trypanosoma brucei, a highly divergent eukaryote. In T. brucei genes are organized in long polycistronic transcription units, drastically reducing the sites of transcription initiation. Employing a highly sensitive and quantitative mass-spectrometry-based approach, we quantified the genome-wide histone acetylation and methylation pattern and identified various acetyl and methyl marks exclusively enriched at TSSs In addition, we show that deletion of histone acetyltransferase 2 results in a loss of H4 acetylation at TSSs, a loss of H2A.Z deposition at TSSs and a shift in the sites of transcription initiation. Combined, our findings demonstrate an evolutionary conserved link between histone H4 acetylation, H2A.Z deposition and RNA transcription initiation.

2020-03-24 | PXD014452 | Pride

H3K4me3 modification profiling of Huntingtons disease and control human post-mortem prefrontal cortex brain samples

Project description:Huntington’s disease (HD) is an autosomal-dominant neurodegenerative disorder resulting from expansion in the number of CAG repeats in the coding region of exon 1 of the Huntingtin (HTT) gene. One of the most widely studied chromatin modifications is trimethylated lysine 4 of histone 3 (H3K4me3). Here, we conducted the first comprehensive study of H3K4me3 ChIP-sequencing in neuronal chromatin from the prefrontal cortex of six HD cases and six non-neurologic controls. We examined two classes of H3K4me3 peaks; those located near transcription start sites (TSSs) (termed “proximal”) and those located distantly from TSSs (termed “distal”). We detected 2,830 differentially enriched H3K4me3 peaks between HD and controls, with 55% of them down regulated in HD. We found an unexpected discordance between levels of H3K4me3 and mRNA, with H3K4me3 predominantly reduced in HD and mRNA predominantly increased in HD. Gene ontology (GO) term enrichment analysis of the genes associated with the proximally positioned peaks, revealed diverse biological process terms with organ morphogenesis and positive regulation of gene expression most frequently implicated. GO terms relating to transcription and the extracellular matrix were also observed. Approximately 36% of the distal peaks co-localized to enhancer sites, with six transcription factors and chromatin remodelers differentially enriched in HD H3K4me3 distal peaks, including EZH2 and SUZ12, two core subunits of the polycomb repressive complex 2 (PRC2). Moreover, sequences repressed by polycomb in normal frontal cortex were significantly depleted in HD-enriched peaks, suggesting that H3K4me3 histone hypermethylation is linked to dysregulated polycomb activity in the HD neuronal epigenome.

2015-12-14 | GSE68952 | GEO

Chromatin architectures at fission yeast transcriptional promoters and replication origins

Project description:We have used micrococcal nuclease (MNase) digestion followed by deep sequencing in order to obtain a higher-resolution map than previously available of nucleosome positions in the fission yeast, Schizosaccharomyces pombe. Our data confirm an unusually short average nucleosome repeat length, ~152 bp, in fission yeast and that transcriptional start sites (TSSs) are associated with nucleosome-depleted regions (NDRs), ordered nucleosome arrays downstream and less regularly spaced upstream nucleosomes. In addition, we found enrichments for associated function in four of eight groups of genes clustered according to chromatin configurations near TSSs. At replication origins, our data revealed asymmetric localization of Pre-Replication Complex (pre-RC) proteins within large NDRsM-bM-^@M-^Ta feature that is conserved in fission and budding yeast and is therefore likely to be conserved in other eukaryotic organisms. Examination of nucleosome positioning in Schizosaccharomyces pombe

2012-04-23 | E-GEOD-28071 | biostudies-arrayexpress

Chromatin architectures at fission yeast transcriptional promoters and replication origins

Project description:We have used micrococcal nuclease (MNase) digestion followed by deep sequencing in order to obtain a higher-resolution map than previously available of nucleosome positions in the fission yeast, Schizosaccharomyces pombe. Our data confirm an unusually short average nucleosome repeat length, ~152 bp, in fission yeast and that transcriptional start sites (TSSs) are associated with nucleosome-depleted regions (NDRs), ordered nucleosome arrays downstream and less regularly spaced upstream nucleosomes. In addition, we found enrichments for associated function in four of eight groups of genes clustered according to chromatin configurations near TSSs. At replication origins, our data revealed asymmetric localization of Pre-Replication Complex (pre-RC) proteins within large NDRs—a feature that is conserved in fission and budding yeast and is therefore likely to be conserved in other eukaryotic organisms.

2012-04-24 | GSE28071 | GEO

Genome-wide maps of IRF3 and YAP in gastric cancer cells.

Project description:We performed chromatin immunoprecipitation (ChIP) assays with YAP and IRF3 antibodies in HGC-27 cells. Analysis of the distribution of YAP- or IRF3-binding sites relative to genes annotated in the human genome, revealed that only a minute fraction of peaks mapped close (<1 kb) to transcription start sites (TSSs) whereas most peaks were located farther than 10 kb from the closest TSS. A total of 6,277 peaks were identified by both YAP and IRF3 antibodies.

2021-11-01 | GSE109081 | GEO

Upstream Anti-sense Promoters Act as Local Enhancers of Mammalian Protein-coding Genes

Project description:Anti-sense transcription originating upstream of mammalian protein-coding genes is a well-documented phenomenon, but remarkably little is known about the function or regulation of these anti-sense promoters or the non-coding RNAs they generate. Here we define at nucleotide resolution the divergent transcription start sites (TSSs) near mouse mRNAs. We find that coupled sense and anti-sense TSSs form the boundaries of an evolutionarily conserved and nucleosome-depleted regulatory region with dramatically enriched transcription factor (TF) occupancy. Notably, as the distance between sense and anti-sense TSSs increases, so does the level of TF binding and signal-dependent gene activation. We further discover a cluster of anti-sense TSSs in macrophages with an enhancer-like chromatin signature. Remarkably, this signature identifies promoters that are selectively and rapidly activated during immune challenge. We conclude that anti-sense TSSs can serve as potent, local enhancers of sense-strand gene expression by facilitating TF binding and deposition of activating histone modifications.

2015-06-23 | GSE62151 | GEO

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