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Genes Dev. 2018 Feb 1;32(3-4):224-229. doi: 10.1101/gad.306464.117. Epub 2018 Feb 26.

A mechanism for epigenetic control of DNA replication.

Author information

1
Oklahoma Medical Research Foundation, Cell Cycle and Cancer Biology Research Program, Oklahoma City, Oklahoma 73104, USA.
2
University of Oklahoma Health Sciences Center, Department of Cell Biology, Oklahoma City, Oklahoma 73104, USA.

Abstract

DNA replication origins in hyperacetylated euchromatin fire preferentially during early S phase. However, how acetylation controls DNA replication timing is unknown. TICRR/TRESLIN is an essential protein required for the initiation of DNA replication. Here, we report that TICRR physically interacts with the acetyl-histone binding bromodomain (BRD) and extraterminal (BET) proteins BRD2 and BRD4. Abrogation of this interaction impairs TICRR binding to acetylated chromatin and disrupts normal S-phase progression. Our data reveal a novel function for BET proteins and establish the TICRR-BET interaction as a potential mechanism for epigenetic control of DNA replication.

KEYWORDS:

DNA replication; DNA replication initiation; bromodomain; chromatin; epigenetic; histone acetylation

PMID:
29483155
PMCID:
PMC5859964
DOI:
10.1101/gad.306464.117
[Indexed for MEDLINE]
Free PMC Article

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