Evidence for the lack of mismatch-repair directed antirecombination during mouse meiosis
- Resource Type
- Authors
- Jian Qin; H te Riele; R. M. Liskay; Sean M. Baker; Norman Arnheim
- Source
- The Journal of heredity. 93(3)
- Subject
- Male
congenital, hereditary, and neonatal diseases and abnormalities
DNA Repair
Base Pair Mismatch
Cell
Biology
Mice
Meiosis
Proto-Oncogene Proteins
Genetics
medicine
PMS2
Animals
Molecular Biology
Genetics (clinical)
Gene knockout
DNA Primers
Mismatch Repair Endonuclease PMS2
Adenosine Triphosphatases
Mice, Knockout
Recombination, Genetic
Base Sequence
Molecular biology
Spermatozoa
digestive system diseases
DNA-Binding Proteins
medicine.anatomical_structure
DNA Repair Enzymes
MutS Homolog 2 Protein
MSH2
DNA mismatch repair
Homologous recombination
Recombination
Biotechnology
- Language
- ISSN
- 0022-1503
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.