Originally published as Genetics Published Articles Ahead of Print on May 5, 2008.

Genetics, Vol. 179, 199-211, May 2008, Copyright © 2008
doi:10.1534/genetics.108.087189

Mechanisms of Rad52-Independent Spontaneous and UV-Induced Mitotic Recombination in Saccharomyces cerevisiae

* Department of Biology and Rosenstiel Center, Brandeis University, Waltham, Massachusetts 02454-9110 and {dagger} CEA, DSV, iRCM, UMR217-CNRS, LERA, Fontenay-aux-Roses, F-92265, France

4 Corresponding author: Rosenstiel Basic Medical Sciences Research Center, MS029, Brandeis University, 415 South St., Waltham, MA 02454-9110.
E-mail: haber{at}brandeis.edu

In wild-type diploid cells, heteroallelic recombination between his4A and his4C alleles leads mostly to His+ gene conversions that have a parental configuration of flanking markers, but ~22% of recombinants have associated reciprocal crossovers. In rad52 strains, gene conversion is reduced 75-fold and the majority of His+ recombinants are crossover associated, with the largest class being half-crossovers in which the other participating chromatid is lost. We report that UV irradiating rad52 cells results in an increase in overall recombination frequency, comparable to increases induced in wild-type (WT) cells, and surprisingly results in a pattern of recombination products quite similar to RAD52 cells: gene conversion without exchange is favored, and the number of 2n – 1 events is markedly reduced. Both spontaneous and UV-induced RAD52-independent recombination depends strongly on Rad50, whereas rad50 has no effect in cells restored to RAD52. The high level of noncrossover gene conversion outcomes in UV-induced rad52 cells depends on Rad51, but not on Rad59. Those outcomes also rely on the UV-inducible kinase Dun1 and Dun1's target, the repressor Crt1, whereas gene conversion events arising spontaneously depend on Rad59 and Crt1. Thus, there are at least two Rad52-independent recombination pathways in budding yeast.


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