Yeast Genetics and Molecular Biology 1998
College Park, Maryland
August 1998


Name: Crouse, Gray F.
Mailing Address: Department of Biology, Emory University, 1510 Clifton Rd., Atlanta, GA 30322, USA
Email Address: gcrouse@biology.emory.edu
Phone and Fax numbers: 404-727-4236, 404-727-2880

036

The role of mismatch repair in prevention of base pair mutations in Saccharomyces cerevisiae .


Gray F. Crouse , Marie C. Earley
Department of Biology, Emory University, 1510 Clifton Rd., Atlanta, GA 30322, USA

We have measured reversion rates of specific base pair mutations in the presence and absence of mismatch repair in S. cerevisiae . Our assay uses six isogenic strains each with a different point mutation in the CYC1 gene that renders the protein non-functional. Only true revertants give a Cyc+ phenotype. We have deleted MSH2 , MSH3 , and MSH6 separately in each of these strains. The reversion rates of three strains were not increased in the absence of mismatch repair. The reversion rates of the other three strains were increased nearly 1000-fold or more in the absence of either MSH2 or MSH6 . We hypothesize that the high reversion rates are due to misincorporations across from damaged bases. To determine if reversion rates were affected by oxidative damage, we grew the strains with high reversion rates in an anaerobic environment, which decreased the reversion rates of the three strains as much as 100-fold. The mutations that give rise to the reversions in these strains are commonly found in cells under oxidative attack. These results suggest that a major function of the mismatch repair system in yeast is to prevent mutations due to misincorporation across from at least some damaged bases. We suggest that this function and the prevention of mutations due to slipped mispairing are the two major repair functions for mismatch repair and that the repair of single base mismatches in undamaged DNA is a relatively minor role.


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