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Deciphering H3K4me3 Broad Domains Associated With Gene Regulatory Networks and Conserved Epigenomic Landscapes in the Human Brain [RNA-Seq]

ABSTRACT: Trimethylated histone H3-lysine 4 is primarily distributed in the form of sharp peaks, extending in neuronal chromatin on average only across 500-1500 base pairs mostly in close proximity to annotated transcription start sites. To explore whether H3K4me3 peaks could also extend across much broader domains, we undertook a detailed analysis of broadest domain cell-type specific H3K4me3 peaks in ChIP-seq datasets from sorted neuronal and non-neuronal nuclei in human, non-human primate and mouse prefrontal cortex (PFC), and blood for comparison. We collected separately cortical gray (GM) and subcortical white matter (WM) from 6 adult human subjects without neurological disease and extracted total RNA processed by the RNA-Seq approach.

ORGANISM(S): Homo sapiens

SUBMITTER: Aslihan Dincer

PROVIDER: E-GEOD-72930 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Deciphering H3K4me3 Broad Domains Associated With Gene Regulatory Networks and Conserved Epigenomic Landscapes in the Human Brain [ChIP-Seq]

Project description:Trimethylated histone H3-lysine 4 is primarily distributed in the form of sharp peaks, extending in neuronal chromatin on average only across 500-1500 base pairs mostly in close proximity to annotated transcription start sites. To explore whether H3K4me3 peaks could also extend across much broader domains, we undertook a detailed analysis of broadest domain cell-type specific H3K4me3 peaks in ChIP-seq datasets from sorted neuronal and non-neuronal nuclei in human, non-human primate and mouse prefrontal cortex (PFC), and blood for comparison. In this GEO submission, we list six newly generated ChIP-seq data sets. FACS sorted Neuronal (NeuN+) nuclei and non-neuronal (NeuN-) nuclei collected from prefrontal cortex (PFC) and processed by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq). In addition we collected nucleated blood cells from 3 control subjects. These are additional subjects unrelated to brain cohort.

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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.

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