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The Chromosome Bias of Misincorporations During Double-Strand Break Repair Is Not Altered in Mismatch Repair–Defective Strains of Saccharomyces cerevisiae
Carolyn B. McGilla, Susan L. Holbecka, and Jeffrey N. Strathernaa Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute–Frederick Cancer Research and Development Center, ABL–Basic Research Program, Frederick, Maryland 21702-1201
Corresponding author: Jeffrey N. Strathern, Gene Regulation and Chromosome Biology Laboratory, NCI-Frederick Cancer Research and Development Center, ABL-Basic Research Program, Box B, Bldg. 539, Frederick, MD 21702-1201, strather{at}ncifcrf.gov (E-mail).
Recombinational repair of a site-specific, double-strand DNA break (DSB) results in increased reversion frequency for nearby mutations. Although some models for DSB repair predict that newly synthesized DNA will be inherited equally by both the originally broken chromosome and the chromosome that served as a template, the DNA synthesis errors are almost exclusively found on the chromosome that had the original DSB (introduced by the HO endonuclease). To determine whether mismatch repair acts on the template chromosome in a directed fashion to restore mismatches to the initial sequence, these experiments were repeated in mismatch repair-defective (pms1, mlh1, and msh2) backgrounds. The results suggest that mismatch repair is not responsible for the observed bias.
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