A mechanism for epigenetic control of DNA replication

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

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle Proteins / chemistry
  • Cell Cycle Proteins / metabolism*
  • Cell Line
  • Chromatin / metabolism
  • DNA Replication*
  • Epigenesis, Genetic*
  • Humans
  • Nuclear Proteins / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • S Phase
  • Transcription Factors / metabolism

Substances

  • BRD2 protein, human
  • BRD4 protein, human
  • Cell Cycle Proteins
  • Chromatin
  • Nuclear Proteins
  • TICRR protein, human
  • Transcription Factors
  • Protein Serine-Threonine Kinases