Selective DNA repair in expressed genes in mammalian cells

For the past decade the authors focused the authors' research upon the intragenomic fine structure of DNA repair in mammalian cells with intent to understand some of the biological phenomena that result from DAN damaging treatments. The authors were particularly interested to understand why cellular sensitivity to agents such as UV does not always correlate with measured efficiencies of DNA repair. A classic example is seen in the comparative UV-sensitivity of human vs. rodent cells and their corresponding DNA repair efficiencies. Although human and mouse fibroblasts in culture exhibit identical UV survival characteristics, the human cells remove most of the cyclobutane pyrimidine dimers (the predominant lesion produced) while the rodent cells remove less than 20%. In this paper, the authors hypothesized that the rodent cells achieve UV-resistance by selective repair of their essential genes in spite of their otherwise low overall repair efficiencies. The experimental documentation of preferential repair of pyrimidine dimers in active genes supports this interpretation