Rad54 dissociates homologous recombination intermediates by branch migration

Dmitry V. Bugreev, Fumio Hanaoka, Alexander V. Mazin

Research output: Contribution to journalArticlepeer-review

83 Scopus citations


Double-strand DNA breaks (DSBs) cause cell death and genome instability. Homologous recombination is a major DSB repair pathway that operates by forming joint molecules with homologous DNA sequences, which are used as templates to achieve accurate repair. In eukaryotes, Rad51 protein (RecA homolog) searches for homologous sequences and catalyzes the formation of joint molecules (D-loops). Once joint molecules have been formed, DNA polymerase extends the 3′ single-stranded DNA tails of the broken chromosome, restoring the lost information. How joint molecules subsequently dissociate is unknown. We reconstituted DSB repair in vitro using purified human homologous recombination proteins and DNA polymerase η. We found that Rad54 protein, owing to its ATP-dependent branch-migration activity, can cause dissociation of joint molecules. These results suggest a previously uncharacterized mechanism of DSB repair in which Rad54 branch-migration activity plays an important role.

Original languageEnglish (US)
Pages (from-to)746-753
Number of pages8
JournalNature Structural and Molecular Biology
Issue number8
StatePublished - Aug 2007
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Structural Biology


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