Saccharomyces cerevisiae mutants lacking the structure-specific nuclease Ra
d27 display an enhancement in recombination that increases as sequence leng
th decreases, suggesting that Rad27 preferentially restricts recombination
between short sequences. Since wild-type alleles of both RAD27 and its huma
n homologue FEN1 complement the elevated short-sequence recombination (SSR)
phenotype of a rad27-null mutant, this function may be conserved from yeas
t to humans. Furthermore, mutant Rad27 and FEN-1 enzymes,vith partial flap
endonuclease activity but without nick specific exonuclease activity partia
lly complement the SSR phenotype of the rad27-null mutant. This suggests th
at the endonuclease activity of Rad27 (FEN-1) plays a role in limiting reco
mbination between short sequences in eukaryotic cells.