Novel function of Rad27 (FEN-1) in restricting short-sequence recombination.
Saccharomyces cerevisiae mutants lacking the structure-specific nuclease Rad27 display an enhancement in recombination that increases as sequence length decreases, suggesting that Rad27 preferentially restricts recombination between short sequences. Since wild-type alleles of both RAD27 and its human homologue FEN1 complement the elevated short-sequence recombination (SSR) phenotype of a rad27-null mutant, this function may be conserved from yeast to humans. Furthermore, mutant Rad27 and FEN-1 enzymes with partial flap endonuclease activity but without nick-specific exonuclease activity partially complement the SSR phenotype of the rad27-null mutant. This suggests that the endonuclease activity of Rad27 (FEN-1) plays a role in limiting recombination between short sequences in eukaryotic cells.
Department of Molecular Biology, Beckman Research Institute, Duarte, California 91010-0269, USA.
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MC
Negritto
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J
Qiu
D O
DO
Ratay
B
B
Shen
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Bailis
D004260:DNA Repair; D004271:DNA, Fungal / Q000235:genetics; D004706:Endodeoxyribonucleases / Q000235:genetics*; D045585:Flap Endonucleases; D009154:Mutation; D011995:Recombination, Genetic; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins
D004271:DNA, Fungal; D029701:Saccharomyces cerevisiae Proteins; D004706:Endodeoxyribonucleases; D045585:Flap Endonucleases; C468317:FEN1 protein, human; C468323:RAD27 protein, S cerevisiae