Replication fork reversal and the maintenance of genome stability

John Atkinson, Peter McGlynn

Research output: Contribution to journalArticle

147 Citations (Scopus)
3 Downloads (Pure)

Abstract

The progress of replication forks is often threatened in vivo, both by DNA damage and by proteins bound to the template. Blocked forks must somehow be restarted, and the original blockage cleared, in order to complete genome duplication, implying that blocked fork processing may be critical for genome stability. One possible pathway that might allow processing and restart of blocked forks, replication fork reversal, involves the unwinding of blocked forks to form four-stranded structures resembling Holliday junctions. This concept has gained increasing popularity recently based on the ability of such processing to explain many genetic observations, the detection of unwound fork structures in vivo and the identification of enzymes that have the capacity to catalyse fork regression in vitro. Here, we discuss the contexts in which fork regression might occur, the factors that may promote such a reaction and the possible roles of replication fork unwinding in normal DNA metabolism.

Original languageEnglish
Pages (from-to)3475-3492
Number of pages18
JournalNucleic Acids Research
Volume37
Issue number11
Early online date30 Apr 2009
DOIs
Publication statusPublished - Jun 2009

Keywords

  • irradiated escherichia-coli
  • blooms-syndrome helicase
  • S-phase checkpoint
  • gross chromosomal rearrangements
  • holliday junction formation
  • nucleotide excision-repair
  • recombination protein recg
  • branch migration protein
  • double-strand breaks
  • DNA-replication

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