The role of the HCR system in the repair of prelethal lesions induced by UV-light, gamma-rays and alkylating agents was studied in the Bacillus subtilis SPP1 phage, its thermosensitive mutants (N3, N73 and ts1) and corresponding infectious DNA. The survival of phages and their transfecting DNA after treatment with UV light is substantially higher in hcr+ cells than in hcr cells, the differences being more striking in intact phages than in their transfecting DNA's. Repair inhibitors reduce the survival in hcr+ cells: caffeine lowers the survival of UV-irradiated phage SPP1 in exponentially growing hcr+ cells but has no effect on its survival in competent hcr+ cells; acriflavin and ethidium bromide decrease the survival of UV-irradiated SPP1 phage in both exponentially growing and competent hcr+ cells to the level of survival observed in hcr cells; moreover, ethidium bromide lowers the number of infective centres in hcr+ cells of UV-irradiated DNA of the SPP1 phage. Repair inhibitors do not lower the survival of UV-irradiated phages or their DNA in hcr cells. The repair mechanism under study repairs also lesions induced by polyfunctional alkylating agents in transfecting DNA's of B. subtilis phages but is not functional with lesions induced by these agents in free phages and lesions caused in phages and their DNA by ethyl methanesulphonate or gamma-rays.

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