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Cell. 2016 Apr 21;165(3):580-92. doi: 10.1016/j.cell.2016.02.062. Epub 2016 Apr 7.

Transcriptional Regulators Compete with Nucleosomes Post-replication.

Author information

1
Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA; Howard Hughes Medical Institute, Seattle, WA 98109, USA.
2
Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA; Howard Hughes Medical Institute, Seattle, WA 98109, USA. Electronic address: steveh@fhcrc.org.

Abstract

Every nucleosome across the genome must be disrupted and reformed when the replication fork passes, but how chromatin organization is re-established following replication is unknown. To address this problem, we have developed Mapping In vivo Nascent Chromatin with EdU and sequencing (MINCE-seq) to characterize the genome-wide location of nucleosomes and other chromatin proteins behind replication forks at high temporal and spatial resolution. We find that the characteristic chromatin landscape at Drosophila promoters and enhancers is lost upon replication. The most conspicuous changes are at promoters that have high levels of RNA polymerase II (RNAPII) stalling and DNA accessibility and show specific enrichment for the BRM remodeler. Enhancer chromatin is also disrupted during replication, suggesting a role for transcription factor (TF) competition in nucleosome re-establishment. Thus, the characteristic nucleosome landscape emerges from a uniformly packaged genome by the action of TFs, RNAPII, and remodelers minutes after replication fork passage.

PMID:
27062929
PMCID:
PMC4855302
DOI:
10.1016/j.cell.2016.02.062
[Indexed for MEDLINE]
Free PMC Article

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