Rad54 dissociates homologous recombination intermediates by branch migration

Nat Struct Mol Biol. 2007 Aug;14(8):746-53. doi: 10.1038/nsmb1268. Epub 2007 Jul 29.


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 eta. 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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • DNA / metabolism
  • DNA Breaks, Double-Stranded*
  • DNA Helicases
  • DNA Repair
  • DNA-Binding Proteins / metabolism
  • Humans
  • Nuclear Proteins / chemistry
  • Nuclear Proteins / physiology*
  • Rad51 Recombinase / physiology
  • Recombination, Genetic / physiology*


  • DNA-Binding Proteins
  • Nuclear Proteins
  • DNA
  • RAD51 protein, human
  • Rad51 Recombinase
  • DNA Helicases
  • RAD54L protein, human