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Genetic Factors in Escherichia coli That Affect Cell Killing and Mutagenesis Induced by Benzo(a)pyrene-7,8-dihydrodiol 9,10-Oxide¹

Cancer Center/Institute of Cancer Research [V. I., & I. B. W.], and Division of Environmental Sciences [I. B. W.], College of Physicians and Surgeons, Columbia University, New York, New York 10032

In the present study, the induction of base-pair reversion mutations from trp to Trp⁺ in the wild type and in uvrA, recA, and lexA mutants of Escherichia coli B/r was used to analyze the mechanism of benzo(a)pyrene-7,8-dihydrodiol 9,10-oxide (BPDE) mutagenesis. BPDE mutagenesis was compared to that of two well characterized mutagens: ethyl methanesulfonate and 4-nitroquinoline 1-oxide. We found that a uvrA mutant was about 20 times more sensitive to BPDE killing and BPDE-induced mutations than was wild-type E. coli. This suggests that BPDE-DNA lesions are removed by an excision repair mechanism similar to that which excises pyrimidine dimers. Although strains carrying either recA or lexA mutations were also more sensitive to BPDE killing, BPDE was not mutagenic in these strains. The recA⁺ and lexA⁺ gene products coordinately control the regulation of a set of genes that are expressed in response to DNA-damaging agents (SOS functions). Therefore, our results indicate that in E. coli BPDE is an indirect mutagen that acts through host-mediated functions, i.e., the SOS pathway, in the process of mutation fixation. The possible significance of these findings to carcinogenesis are discussed.

¹ This investigation was supported by Grant CA-21111-03 from the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 2/ 4/80. Accepted 6/26/80.