Abstract
In the presence of acridine orange (AO) and monochromatic 500-nm light, the recombination-deficient strain of Escherichia coli, WP10 ( recA), showed a 15-fold increase in mutation rate over the wild-type (WP2) strain. Under the same conditions, strain B s−1 ( uvrB lesA lon) showed a 5-fold increase in mutation rate over strain WP2. In contrast, the endonuclease-deficient strain, WP2s ( uvrA), showed a lower AO-500 nm mutation rate than wild-type. The extremely high mutation rate of the recA strain cannot be due to error-prone inducible SOS repair since the inducible recA + function is absent. Repair of the AO-500 nm-induced lesions is likely due to a recA +-dependent, error-free, recombination process. It is concluded that the high mutation rates with AO-500 nm light obtained in chemostat cultures of recA ad lexA strains occur as a consequence of errors during semi-conservative DNA replication in the presence of unrepaired DNA lesions.
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More From: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
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