A mechanism for epigenetic control of DNA replication
- Courtney G. Sansam1,
- Katarzyna Pietrzak1,
- Blanka Majchrzycka1,
- Maciej A. Kerlin1,
- Jingrong Chen1,
- Susannah Rankin1,2 and
- Christopher L. Sansam1,2
- 1Oklahoma Medical Research Foundation, Cell Cycle and Cancer Biology Research Program, Oklahoma City, Oklahoma 73104, USA;
- 2University of Oklahoma Health Sciences Center, Department of Cell Biology, Oklahoma City, Oklahoma 73104, USA
- Corresponding author: chris-sansam{at}omrf.org
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.
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Footnotes
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Supplemental material is available for this article.
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Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.306464.117.
- Received August 25, 2017.
- Accepted January 23, 2018.
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