Repair of haloethylnitrosourea-induced DNA damage in mutant and adapted bacteria.
The sensitivities of Escherichia coli K-12 strain AB1157, its uvrA-deficient mutant AB1886, and its recA mutant AB2463 to N,N'-bis(2-chloroethyl)-N-nitrosourea, N-(2-chloroethyl)-N-nitrosourea, and N-ethyl-N-nitrosourea have been determined. These data indicate that loss of either uvr excision repair or recA-dependent DNA repair greatly increases sensitivity to the haloethylnitrosoureas. At the same time, loss of recA-dependent DNA repair increases sensitivity to N-ethyl-N-nitrosourea significantly while loss of uvr excision repair increases sensitivity to this agent only marginally. Adapting the uvrA-deficient and recA-deficient mutants by growth in N-methyl-N'-nitro-N-nitrosoguanidine increases survival after exposure to either N-methyl-N'-nitro-N-nitrosoguanidine or N-ethyl-N-nitrosourea, but neither adapted strain loses its sensitivity to N,N'-bis(2-chloroethyl)-N-nitrosourea. Taken together, these data indicate that the haloethylnitrosoureas cause other important cytotoxic lesions in DNA in addition to those involving alkylation of the O6 position of guanine and that the uvrA and recA gene products are involved in the repair of these lesions.[1]References
- Repair of haloethylnitrosourea-induced DNA damage in mutant and adapted bacteria. Kacinski, B.M., Rupp, W.D., Ludlum, D.B. Cancer Res. (1985) [Pubmed]
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