Replication and repair of UV-induced mutational lesions in chemostat cultures of Escherichia coli WP2 Hcr

Mutation to resistance to bacteriophage T5 was studied in chemostat cultures of Escherichia coli strain WP2 Hcr exposed to ultraviolet radiation (UV). The results are in generally good agreement with those obtained earlier by Bridges and Munson for UV-induced reversion to tryptophan independence in exponentially growing cultures of the same strain: expressed mutant yields followed a dose-squared response, mutations were not expressed before approximately one generation after exposure to UV, there was a slow disappearance of dimers especially noticeable in slowly growing and stationary cultures, and the first replication gave rise to duplex mutants in both strands. Several new results were also obtained. In addition to expressed mutant yields, induction of mutational capacity was also observed to follow a dose-squared response, indcating that the response is not an artifact of selection or repair. Induction also increased with growth rate, apparently as the square of the number of genes for T5-sensitivity per cell. It is suggested that mutagenesis is proportional to the number of genes per cell, that recombination is also proportional to the number of genes per cell, and that the number of mutational lesions is proportional to the product of the two. These results also provide evidence that DNA replication occurs near the end of the cell cycle in slowly growing cultures. Under all growth conditions, latent mutant concentrations mutational capacity) decreased by a factor of two with each successive division. Latent mutants were, however, photoreversible for only the first two generations. If mutagenesis occurs as a recombinant event between two mutational lesions, then the results also indicate that these lesions are separated, on the average, by no more than a single cistron.