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Abstract
In the budding yeast Saccharomyces cerevisiae, null alleles of several DNA repair and recombination genes confer defects in recombination that grow more severe with decreasing sequence length, indicating that they are required for short-sequence recombination (SSR). RAD1 and RAD10, which encode the subunits of the structure-specific endonuclease Rad1/10, are critical for SSR. MRE11, RAD50, and XRS2, which encode the subunits of M/R/X, another complex with nuclease activity, are also crucially important. Genetic evidence suggests that Rad1/10 and M/R/X act on the same class of substrates during SSR. MSH2 and MSH3, which encode subunits of Msh2/3, a complex active during mismatch repair and recombination, are also important for SSR but play a more restricted role. Additional evidence suggests that SSR is distinct from nonhomologous end joining and is superimposed upon basal homologous recombination.
This work was supported by U.S. Public Health Service grant GM57484 to A.M.B., as well as funds from the Beckman Research Institute of the City of Hope and the City of Hope National Medical Center.
We thank J. McDonald, E. Alani, N. Kleckner, R. D. Kolodner, K. Shannon, D. T. Weaver, S. Moreau, L. Symington, D. Bressan, J. Petrini, J. Nickoloff, and B. Jensen for strains and plasmids. We also thank P. Sung, J. Petrini, J. Haber, and the members of the Bailis laboratory for stimulating discussions. Finally, we thank D. Bishop and several anonymous reviewers for insightful comments on the manuscript.