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Molecular and Cellular Biology, April 2001, p. 2349-2358, Vol. 21, No. 7
Department of Molecular Biology, Beckman
Research Institute,1 and Department
of Cell and Tumor Biology, City of Hope National Medical
Center,2 Duarte, California 91010-0269
Received 1 December 2000/Returned for modification 6 January
2001/Accepted 15 January 2001
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.
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.7.2349-2358.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Novel Function of Rad27 (FEN-1) in
Restricting Short-Sequence Recombination
*
Corresponding author. Mailing address: Department of
Molecular Biology, Beckman Institute of the City of Hope, 1450 E. Duarte Rd., Duarte, CA 91010-0269. Phone: (626) 359-8111, ext. 64031. Fax: (626) 301-8271. E-mail: abailis{at}coh.org.
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