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Nucleic Acids Research 2004 32(14):4257-4268; doi:10.1093/nar/gkh717
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Published online 10 August 2004

Nucleic Acids Research, Vol. 32 No. 14 © Oxford University Press 2004; all rights reserved

The DNA damage checkpoint pathways exert multiple controls on the efficiency and outcome of the repair of a double-stranded DNA gap

Edwin Haghnazari1 and Wolf-Dietrich Heyer1,2,3,*

1 Division of Biological Sciences and Section of Microbiology, 2 Section of Molecular and Cellular Biology and 3 Center for Genetics and Development, University of California, Davis, CA 95616-8665, USA

* To whom correspondence should be addressed. Tel: +1 530 752 3001; Fax: +1 530 752 3011; Email: wdheyer{at}ucdavis.edu

Received June 8, 2004; Revised and Accepted July 4, 2004

A DNA gap repair assay was used to determine the effect of mutations in the DNA damage checkpoint system on the efficiency and outcome (crossover/non-crossover) of recombinational DNA repair. In Saccharomyces cerevisiae gap repair is largely achieved by homologous recombination. As a result the plasmid either integrates into the chromosome (indicative of a crossover outcome) or remains extrachromosomal (indicative of a non-crossover outcome). Deletion mutants of the MEC1 and RAD53 checkpoint kinase genes exhibited a 5-fold decrease in gap repair efficiency, showing that 80% of the gap repair events depended on functional DNA damage checkpoints. Epistasis analysis suggests that the DNA damage checkpoints affect gap repair by modulating Rad51 protein-mediated homologous recombination. While in wild-type cells only ~25% of the gap repair events were associated with a crossover outcome, Mec1-deficient cells exhibited a >80% crossover association. Also mutations in the effector kinases Rad53, Chk1 and Dun1 were found to affect crossover association of DNA gap repair to various degrees. The data suggest that the DNA damage checkpoints are important for the optimal functioning of recombinational DNA repair with multiple terminal targets to modulate the efficiency and outcome of homologous recombination.


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