Inhibition of DNA synthesis is not sufficient to cause mutagenesis in Chinese hamster cells.

Experiments were designed to test whether the inhibition of DNA synthesis in Chinese hamster V79 cells would result in increased mutagenesis by a mechanism similar to "SOS repair" in E. coli. Treatment of cells for 16 hours with excess of the deoxynucleosides TdR, UdR, AdR and GdR was mutagenic, whereas treatment with hydroxyurea demonstrated no mutagenic effect. The mutagenicity of TdR could be reversed by the addition of CdR. In E. coli, inhibition of DNA synthesis by a short exposure to hydroxyurea resulted in the induction of lambda prophage and increased mutagenesis. These results show that whereas the presence of a stalled replication fork in E. coli can result in mutagenesis via induction of the "SOS system", the same phenomenon does not seem to occur in Chinese hamster V79 cells. The mutagenic mechanism of high concentrations of deoxynucleosides in Chinese hamster V79 cells is likely to be due to replication errors which result from alterations in deoxynucleotide pools.