Histone turnover mediates epigenetic processes in Drosophila S2 cells
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE4091 | GEO | 2007/12/01
SECONDARY ACCESSION(S): PRJNA95249
REPOSITORIES: GEO
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Project description:We developed a system to study the DNA replication-independent turnover nucleosomes containing the histone variant H3.3 in mammalian cells. By measuring the genome-wide incorporation of H3.3 at different time points following epitope-tagged H3.3 expression, we find three categories of H3.3-nucleosome turnover in vivo: rapid turnover, intermediate turnover and, specifically at telomeres, slow turnover. Our data indicate that H3.3-containing nucleosomes at enhancers and promoters undergo a rapid turnover that is associated with active histone modification marks including H3K4me1, H3K4me3, H3K9ac, H3K27ac and the histone variant H2A.Z. The rate of turnover is negatively correlated with H3K27me3 at regulatory regions and with H3K36me3 at gene bodies.
2013-10-23 | GSE51505 | GEO
Project description:Histones of higher eukaryotes are assembled into chromatin primarily during DNA replication, but at other times the histone H3.3 variant replaces canonical H3. We introduce a novel strategy for profiling epigenetic patterns based on H3.3 replacement, using microarrays covering about one third of the Drosophila melanogaster genome at 100-bp resolution. Striking patterns of H3.3 replacement were found over active genes and transposons. H3.3 replacement occurs prominently at sites of abundant RNA polymerase II and methylated H3 lysine-4 throughout the genome, and is enhanced on the dosage-compensated male X chromosome. Active genes are depleted of histones at promoters and are enriched in H3.3 from upstream to downstream of transcription units. Based on these findings, we propose that deposition and inheritance of actively modified H3.3 in regulatory regions maintains transcriptionally active chromatin. Keywords: Chromatin affinity-purification on microarray
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Project description:Turnover and exchange of nucleosomal histones and their variants, a process long believed to be static in post-replicative cells, remains largely unexplored in brain. Here, we describe a novel mechanistic role for HIRA (histone cell cycle regulator) and proteasomal degradation associated histone dynamics in the regulation of activity-dependent transcription, synaptic connectivity and behavior. We uncover a dramatic developmental profile of nucleosome occupancy across the lifespan of both rodents and humans, with the histone variant H3.3 accumulating to near saturating levels throughout the neuronal genome by mid-adolescence. Despite such accumulation, H3.3 containing nucleosomes remain highly dynamic–in a modification independent manner–to control neuronal- and glial- specific gene expression patterns throughout life. Manipulating H3.3 dynamics in both embryonic and adult neurons confirmed its essential role in neuronal plasticity and cognition. Our findings establish histone turnover as a critical, and previously undocumented, regulator of cell-type specific transcription and plasticity in mammalian brain. All ChIP-seq samples were generated to test the impact of neuronal activity/adult physiological plasticity on histone turnover in the central nervous system. This was tested in cultured neurons and astrocytes, FACS purified neurons or FACS purified Glia.
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2015-06-23 | E-GEOD-69807 | biostudies-arrayexpress
Project description:Epigenetic environment of histone H3.3 on promoters revealed by integration of imaging and genome-scale chromatin and methyl-DNA immunoprecipitation information. Chromatin regions with different transcriptional outputs are distinguished by the deposition of histone variants. Histone H3.3 is incorporated into chromatin in a replication-independent manner; yet the relationship between H3.3 deposition, chromatin environment is incompletely understood. We have integrated imaging and genome-scale chromatin and methyl-DNA immunoprecipitation approaches to investigate the genomic distribution of epitope-tagged H3.3 in relation to histone modifications, DNA methylation and transcription. Results: Imaging shows that H3.3, in contrast to replicative H3.1 or H2B, is enriched in chromatin marked by histone modifications of active genes. A genome-wide survey identifies 1,649 H3.3-enriched promoters, only a subset of which is co-enriched in H3K4me3, H3K9me3 and/or H3K27me3, with a preference for H3K4me3, corroborating imaging data. H3.3-enriched promoters are depleted of H3.3 at the TSS in a transcription-independent manner. H3.3 is found predominantly on CpG-rich unmethylated promoters, creating a condition favourable for transcription. In undifferentiated mesenchymal stem cells, H3.3 target genes are linked to signaling and mesodermal differentiation, suggesting that H3.3 may be a mark of lineage priming. Conclusions: A minor fraction of H3.3 is targeted to promoters, which are predominantly CpG-rich, DNA unmethylated and devoid of detectable trimethylated H3K4, K9 and K27. Among H3.3 target promoters co-marked by methylated H3, H4K4me3 is preferred, with or without H3K27me3, arguing that in mesenchymal stem cells H3.3 marks transcriptionally active or potentially active promoters. Key words: Imaging, ChIP-chip, MeDIP-chip, histone H3.3, mesenchymal stem cells ChIP-chip and MeDIP-chip experiments: Performed with two independent biological replicates. Gene expression profiling experiments: Total RNA obtained from H3.3-EGFP transfected or empty-EGFP transfected mesenchymal stem cells compared to untransfected mesenchymal stem cells. Raw expression data linked below as supplementary file (GSE17053_Illumina_non-normalized_data.txt).
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Project description:Establishment of a proper chromatin landscape is central to genome function. Here, we explain H3 variant distribution by specific targeting and dynamics of deposition involving the CAF-1 and HIRA histone chaperones. Impairing replicative H3.1 incorporation via CAF-1 enables an alternative H3.3 deposition at replication sites via HIRA. Conversely, the H3.3 incorporation throughout the cell cycle via HIRA cannot be replaced by H3.1. ChIP-seq analyses reveal correlation between HIRA-dependent H3.3 accumulation and RNA pol II at transcription sites and specific regulatory elements, further supported by their biochemical association. Remarkably, the HIRA complex shows unique DNA binding properties and depleting HIRA increases DNA sensitivity to nucleases. We propose that protective gap-filling of naked DNA by HIRA leads to a broad distribution of H3.3, and HIRA association with Pol II ensures local H3.3 enrichment at specific sites. Examination of genome-wide localization of two histone H3 variants.
2011-12-16 | E-GEOD-31794 | biostudies-arrayexpress
Project description:The HIRA chaperone complex, comprised of HIRA, UBN1 and CABIN1, collaborates with histone-binding protein ASF1a to incorporate histone variant H3.3 into chromatin in a DNA replication-independent manner. To better understand its function and mechanism, we integrated HIRA, UBN1, ASF1a and histone H3.3 ChIP-seq and gene expression analyses. Most HIRA-binding sites co-localize with UBN1, ASF1a and H3.3 at active promoters and active and weak/poised enhancers. At promoters, binding of HIRA/UBN1/ASF1a correlates with the level of gene expression. HIRA is required for deposition of histone H3.3 at its binding sites. There are marked differences in nucleosome and co-regulator composition at different classes of HIRA-bound regulatory site. Underscoring this, we report novel physical interactions between the HIRA complex and transcription factors, a chromatin insulator and an ATP-dependent chromatin-remodelling complex. Our results map the distribution of the HIRA chaperone across the chromatin landscape and point to different interacting partners at functionally distinct regulatory sites. Examination of H3.3 histone modification in HeLA cells with accompanying FAIRE data
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Project description:Turnover and exchange of nucleosomal histones and their variants, a process long believed to be static in post-replicative cells, remains largely unexplored in brain. Here, we describe a novel mechanistic role for HIRA (histone cell cycle regulator) and proteasomal degradation associated histone dynamics in the regulation of activity-dependent transcription, synaptic connectivity and behavior. We uncover a dramatic developmental profile of nucleosome occupancy across the lifespan of both rodents and humans, with the histone variant H3.3 accumulating to near saturating levels throughout the neuronal genome by mid-adolescence. Despite such accumulation, H3.3 containing nucleosomes remain highly dynamic–in a modification independent manner–to control neuronal- and glial- specific gene expression patterns throughout life. Manipulating H3.3 dynamics in both embryonic and adult neurons confirmed its essential role in neuronal plasticity and cognition. Our findings establish histone turnover as a critical, and previously undocumented, regulator of cell-type specific transcription and plasticity in mammalian brain.
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