During the experiments, the scientists used a mutant form of RecA, which can not unwind the helix, and then observed how much it affects the different stages of homologous recombination. It turned out that the mutant form successfully recognises the homologous site but is unable to form a D-loop, a three-stranded DNA intermediate structure that requires unwinding of the helix. This result supports the second model of recombination.
Disruption of this mechanism underlies the high incidence of breast cancer in patients with inherited defects in the BRCA1 and BRCA2 genes. They encode proteins that play an important role in repairing DNA damage and are responsible for the correct interaction between single-stranded DNA and RAD51, the human version of the RecA protein.
