TY - JOUR
T1 - Damage-induced ectopic recombination in the yeast Saccharomyces cerevisiae
AU - Kupiec, Martin
AU - Steinlauf, Rivka
N1 - Funding Information:
We thank Mary Vail and Rina Jaget for excellent technical assistance, and the whole Kupiec Laboratory for comments on the manuscript. This work was supported by a grant from the Israel Science Foundation.
PY - 1997/6/9
Y1 - 1997/6/9
N2 - Mitotic recombination in the yeast Saccharomyces cerevisiae is induced when cells are irradiated with UV or X-rays, reflecting the efficient repair of damage by recombinational repair mechanisms. We have used multiply marked haploid strains that allow the simultaneous detection of several types of ectopic recombination events. We show that inter-chromosomal ectopic conversion of lys2 heteroalleles and, to a lesser extent, direct repeat recombination (DRR) between non-tandem repeats, are increased by DNA-damaging agents; in contrast, ectopic recombination of the naturally occurring Ty element is not induced. We have tested several hypotheses that could explain the preferential lack of induction of Ty recombination by DNA-damaging agents. We have found that the lack of induction cannot be explained by a cell cycle control or by an effect of the mating-type genes. We also found no role for the flanking long terminal repeats (LTRs) of the Ty in preventing the induction. Ectopic conversion, DRR, and forward mutation of artificial repeats show different kinetics of induction at various positions of the cell cycle, reflecting different mechanisms of recombination. We discuss the mechanistic and evolutionary aspects of these results.
AB - Mitotic recombination in the yeast Saccharomyces cerevisiae is induced when cells are irradiated with UV or X-rays, reflecting the efficient repair of damage by recombinational repair mechanisms. We have used multiply marked haploid strains that allow the simultaneous detection of several types of ectopic recombination events. We show that inter-chromosomal ectopic conversion of lys2 heteroalleles and, to a lesser extent, direct repeat recombination (DRR) between non-tandem repeats, are increased by DNA-damaging agents; in contrast, ectopic recombination of the naturally occurring Ty element is not induced. We have tested several hypotheses that could explain the preferential lack of induction of Ty recombination by DNA-damaging agents. We have found that the lack of induction cannot be explained by a cell cycle control or by an effect of the mating-type genes. We also found no role for the flanking long terminal repeats (LTRs) of the Ty in preventing the induction. Ectopic conversion, DRR, and forward mutation of artificial repeats show different kinetics of induction at various positions of the cell cycle, reflecting different mechanisms of recombination. We discuss the mechanistic and evolutionary aspects of these results.
KW - Cell cycle
KW - Gene conversion
KW - Genomic stability
KW - Ty element
UR - http://www.scopus.com/inward/record.url?scp=0030926123&partnerID=8YFLogxK
U2 - 10.1016/S0921-8777(97)00012-8
DO - 10.1016/S0921-8777(97)00012-8
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AN - SCOPUS:0030926123
SN - 0921-8777
VL - 384
SP - 33
EP - 44
JO - Mutation Research - DNA Repair
JF - Mutation Research - DNA Repair
IS - 1
ER -