Abstract
We have analyzed delayed mutation as a part of cellular responses to genotoxic damage and found that this occurs at the pink-eyed unstable locus in the somatic cells of F1 mice born to irradiated sperm. However, a whole body mouse system and tissue culture cells are too complex to elucidate the molecular mechanism of delayed mutation.
We have now examined delayed mutation in fission yeast. We constructed tester strains which carry reporter genes with tandem duplications. These reporters can revert to the wild type ura4 through homologous recombination. We mainly tested the strains carrying a pair of 200 bp repeats and found that X-irradiation increased recombination frequency of the reporter loci in a dose dependent manner before restarting from arrested cell cycle. In addition, the activation of recombination persisted for about 10 cell generations after irradiation within which damage repair was thought to have been completed. A Rad51 deficient strain did not exhibit both induction and continuation of high-frequent recombination.
These results suggest that untargeted and delayed activation of recombination system is induced not only in mice but in fission yeast by damage to the genome.
