Abstract
Abstract— We have recently reported that DNA double‐strand breaks arise enzymatically during the course of excision repair in uvr+ strains of Escherichia coli K‐12. Survival curves for ultraviolet (UV) irradiated E. coli K‐12 pol+ (JG139) and polA1 (JG138) strains have a pronounced shoulder region. The regions of the survival curves at which killing approaches exponential correspond to the fiuences at which DNA double‐strand breaks (assumed to be lethal events) accumulate linearly. Reducing the number of UV photoproducts either by photoreactivation or fluence fractionation results in an increase in survival and a decrease in the yield of DNA double‐strand breaks in both strains. These data support the hypothesis that enzymatically‐induced DNA double‐strand breaks may be the lesion ultimately responsible for UV‐induced cell killing in the pol+ strain of E. coli K‐12. and perhaps also in the polA1 strain.