SOS induction by gamma-radiation in Escherichia coli strains defective in repair and/or recombination mechanisms.

Ionizing radiation causes several types of DNA lesions, mainly single- or double-strand breaks and base damage. By means of the chromotest, an assay that allows the level of the SOS response to be monitored via beta-galactosidase enzymatic activity, the roles of several repair (uvrA, recN and oxyR) and recombination (recB, recJ and recO) genes in the response of Escherichia coli to gamma-radiation were studied. The results indicate that all the repair- and recombination-deficient strains were more sensitive to the lethal effects of ionizing radiation. However, the SOS activation pattern was somewhat different. The minimal inducing dose in uvrA and recN mutants was lower than in the wild-type, whereas their SOS response was higher at all doses. Conversely, in the strains lacking an active recB, recJ or recO gene, the doubling dose was almost the same as in the wild-type but the level of induction remained stable over a wide dose range. These findings suggest that neither single- nor double-strand breaks are in themselves direct SOS inducers and that while uvrA, recN and oxyR take part in different repair or protective pathways, apparently recB, recJ and recO participate in damage processing leading to SOS induction, as well as in recombination repair.