The repair of DNA single-strand breaks has been studied in Escherichia coli K-12 (W3110) after X irradiation in the presence and absence of oxygen. Upon completion in buffer of a very fast repair process (Type I) there are three times as many breaks remaining after irradiation in the presence as compared with the absence of oxygen. These breaks are then rapidly repaired in buffer by the Type II system; a process that is deficient in strains carrying the polA1 mutation (an amber mutation in the structural gene for DNA polymerase I). After low doses of x rays, the Type II system can repair all of the breaks presented to it. Beyond a threshold dose it repairs a constant proportion (∼90%) of the breaks presented to it whether or not oxygen is present during irradiation. Consistent with the apparent insensitivity of the Type II repair process to the presence of oxygen during irradiation, otherwise isogenic <tex-math>$pol^{+}$</tex-math> and <tex-math>$pol^{-}$</tex-math> derivatives were found to have the same oxygen enhancement ratio (OER) for cell survival. After Type II repair is complete, some of the remaining breaks can be repaired by the growth-medium-dependent Type III system. This process can repair only about 2 additional breaks per single-strand genome in this strain, whether irradiation is in the presence or absence of oxygen. Thus, as far as the repair of DNA single-strand breaks is concerned, neither the Type II nor the Type III repair system shows any specificity for breaks produced in the presence or absence of oxygen. OER values were determined for the recA and recB mutants which are deficient in Type III repair. While the recB derivative showed only a slight reduction in OER, the recA derivative had an OER of about 2.0 compared with about 3.4 for the rec+ parental strain. Since the recA mutation would affect Type III repair to the same extent whether the cells were x-irradiated in the presence or absence of oxygen, the reduced OER for the recA strain probably reflects the additional involvement of the recA gene product in the repair of some other lesion, possibly based damage, that is affected by the presence of oxygen during irradiation.

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