DNA excision repair as a component of adaptation to low doses of ionizing radiation in Escherichia coli.

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In this study we examined whether or not DNA excision repair is a component of adaptation induced by very low-dose ionizing radiation in Escherichia coli, a well-characterized prokaryote, and investigated the relationship between enhanced excision repair and the SOS response. Competent E. coli cells were irradiated using low doses (0.1-10 Gy) of 137Cs gamma-rays, allowed to recover for 2 h and were then transformed using pUC18 DNA containing approximately 22 oxidized thymine residues (thymine glycols) per molecule. Successful transformants were identified by recovery of plasmid-borne ampicillin resistance and the resulting data (colony counts) were used to calculate ratios of plasmid recovery in irradiated to control cells. Results showed that cells irradiated with very low doses (0.1-0.5 Gy) were up to 30-40% more efficient at utilizing thymine glycol-containing pUC18 DNA. The enhanced excision repair by very low doses (< 0.5 Gy) of gamma-rays was shown to be independent of the recA-controlled SOS response in experiments using recA cells or cells carrying recA-lacZ gene fusions. The stimulating effect in AB1157 prototype cells were subsequently confirmed using a DNA precipitation assay in which DNA incision events were accumulated by inhibiting DNA ligation with ethidium bromide. Our data suggest that there seems to be narrow 'windows' of dose-effect for the induction of SOS-independent DNA excision repair. Being similar to mammalian cell studies, the dose range for this effect was about 200-fold less than D37 for radiation survival.