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The Journal of Heredity 2002:93(3)
© 2002 The American Genetic Association 93:201-205

Brief Communication

Evidence for the Lack of Mismatch-Repair Directed Antirecombination During Mouse Meiosis

J. Qin, S. Baker, H. Te Riele, R. M. Liskay, and N. Arnheim

From the Molecular Biology Program, University of Southern California, 835 West 37th St., Los Angeles, CA 90089-1340 (Qin and Arnheim), Department of Nutritional Science, Morgan Hall 233, University of California at Berkeley, Berkeley, CA 94720-3104 (Baker), Division of Molecular Biology, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands (Te Riele), and Department of Medical and Molecular Genetics, L103, Oregon Health Sciences University, 3181 SW Sam Jackson Park Rd., Portland, OR 97201-3098 (Liskay).

Address correspondence to Norman Arnheim at the address above or e-mail: arnheim{at}usc.edu.

Meiotic recombination was studied in DNA mismatch repair (MMR)-deficient mice using a strain carrying a Pms2 knockout mutation. Using single-sperm typing, recombination was analyzed over five intervals on four chromosomes in four Pms2 -/- animals. A total of 1936 meioses were studied and compared to 1848 meioses from three Pms2 +/+ controls. A smaller study was carried out on a single interval in each of two chromosomes in an MMR-deficient mouse homozygous for the Msh2 knockout mutation. A total of 792 meioses were examined in the Msh2 -/- and 880 meioses in the Msh2 +/+ animal. Recombination fractions were not significantly different in either of the MMR-deficient mouse strains when compared to MMR-proficient controls. Our results appear to conflict with mouse embryonic stem (ES) cell gene-targeting experiments where MMR plays a major role in determining the efficiency of homologous recombination between nonidentical sequences. A number of possibilities could explain the apparent lack of a significant effect on meiosis.


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