Ultraviolet (UV)‐irradiated E. coli K‐12 wild‐type cells were sensitized by a post‐irradiation treatment with 10 ‐2 M 2, 4‐dinitrophenol (DNP). This effect was not seen in strains carrying a uvr mutation, suggesting that DN P interferes with the excision repair process. The polA strain was sensitized to the same extent as the wild‐type strain, while the exrA strain was not affected by DNP treatment. Recombination deficient strains ( recA, recB and recA recB ) were protected by DNP treatment after UV irradiation. This protection was abolished by the addition of a uvr mutation (i.e., in strains recA uvrB and recB uvrB ). Alkaline sucrose gradient sedimentation studies showed that DNP treatment interfered with the rejoining of DNA single‐strand breaks induced by the excision repair process. This interference was apparently specific for the exr gene‐dependent branch of the uvr gene‐dependent excision repair process, since the uvr and exr strains were not sensitized while the wild‐type and polA strains were sensitized.
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Schueren et al. (1974) studied this question.
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