Histone modifications form a cell-type-specific chromosomal bar code that persists through the cell cycle
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA686658 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13276081.fastq.gz | Fastqsanger.gz | |||
| SRR13276082.fastq.gz | Fastqsanger.gz | |||
| SRR13276083_1.fastq.gz | Fastqsanger.gz | |||
| SRR13276083_2.fastq.gz | Fastqsanger.gz | |||
| SRR13276084_1.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin configuration influences gene expression in eukaryotes at multiple levels, from individual nucleosomes to chromatin domains several Mb long. Post-translational modifications (PTM) of core histones seem to be involved in chromatin structural transitions, but how remains unclear. To explore this, we used ChIP-seq and two cell types, HeLa and lymphoblastoid (LCL), to define how changes in chromatin packaging through the cell cycle influence the distributions of three transcription-associated histone modifications, H3K9ac, H3K4me3 and H3K27me3. We show that chromosome regions (bands) of 10-50 Mb, detectable by immunofluorescence microscopy of metaphase (M) chromosomes, are also present in G1 and G2. They comprise 1-5 Mb sub-bands that differ between HeLa and LCL but remain consistent through the cell cycle. The same sub-bands are defined by H3K9ac and H3K4me3, while H3K27me3 spreads more widely. We found little change between cell cycle phases, whether compared by 5 Kb rolling windows or when analysis was restricted to functional elements such as transcription start sites and topologically associating domains. Only a small number of genes showed cell-cycle related changes: at genes encoding proteins involved in mitosis, H3K9 became highly acetylated in G2M, possibly because of ongoing transcription. In conclusion, modified histone isoforms H3K9ac, H3K4me3 and H3K27me3 exhibit a characteristic genomic distribution at resolutions of 1 Mb and below that differs between HeLa and lymphoblastoid cells but remains remarkably consistent through the cell cycle. We suggest that this cell-type-specific chromosomal bar-code is part of a homeostatic mechanism by which cells retain their characteristic gene expression patterns, and hence their identity, through multiple mitoses.
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Project description:Histone post-translational modifications (PTMs) play a critical role in chromatin regulation. It has been proposed that these PTMs form localized “codes” that are read by specialized domains (reader domains) in chromatin associated proteins (CAPs) to regulate downstream function. Substantial effort has been made to define [CAP - histone PTM] specificity, and in doing so to decipher the histone code. However, this has largely been done using a reductive approach of isolated reader domains and histone peptides, with the assumption that PTM readout is unaffected by any higher order considerations. Here we show that histone PTM specificity is in fact dependent on nucleosomal context, necessitating we re-define the ‘histone code’ concept and further interrogate it at the nucleosomal level.
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Project description:Epigenetic modifications and transcription factors form a chromatin code to regulate gene expression in many physiological and pathological processes. However, little is known about whether the environmental stimuli could interplay with this code and regulate the transcription and biological functions. Here, we interrogated the chromatin state of multiple epigenetic modifications and transcription factors during a time course of VEGF stimulation in the endothelial cells and found a broad change of transcriptome induced by VEGF. At the promoter-proximal regions, a unique epigenetic pattern of bivalent domain preferentially governed the part of transcriptome change by hijacking the EZH1 transcriptional activity. VEGF substantially altered the epigenetic landscape at enhancer regions and transcription factor chromatin occupancy across the genome, which significantly accounted for the change of VEGF-downstream gene expression. Moreover, by integrating a transcription-regulatory network of VEGF pathway, we discovered MAFs as a novel mater transcriptional factor controlling the VEGF transcriptional program and angiogenesis. Collectively, these results revealed the extracellular stimulus of VEGF in fact implements a significant reconfiguration of chromatin code that coordinately regulates the angiogenic response.
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