Enhanced mutagenesis of <i>Salmonella</i> tester strains due to deletion of genes other than <i>uvrB</i>

Environmental and Molecular Mutagenesis - Tập 48 Số 8 - Trang 694-705 - 2007
Carol D. Swartz1, Nick Parks2, David M. Umbach3, William O. Ward4, Roel M. Schaaper5, David M. DeMarini4
1Department of Environmental Science and Engineering University of North Carolina Chapel Hill North Carolina USA
2Environmental Careers Organization, Boston, Massachusetts
3Biostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, DHHS, Research Triangle Park, North Carolina
4Environmental Carcinogenesis Division, US Environmental Protection Agency, Research Triangle Park, North Carolina
5Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, DHHS, Research Triangle Park, North Carolina

Tóm tắt

AbstractThe standard Salmonella mutagenicity (Ames) tester strains are missing 15–119 genes due to the extended Δ(gal‐bio‐uvrB) mutations that render the strains excision‐repair deficient (ΔuvrB). We constructed strains of Salmonella that are homologous to tester strains TA98 and TA100 except that in place of the uvrB deletion, they contain single‐gene defects in either uvrB, moaA, moeA, or both uvrB and moeA. We then tested the following mutagens in these strains: 2‐acetylaminofluorene, Glu‐P‐1, 4‐aminobiphenyl, benzo[a]pyrene, MX, 1‐nitropyrene, 6‐hydroxylaminopurine (HAP), and 2‐amino‐6‐hydroxylaminopurine (AHAP). We confirmed in Salmonella a previous finding in Escherichia coli that the enhanced mutagenicity of the purine analogues HAP and AHAP is not due to the deletion of the uvrB gene but due to the deletion of moeA and/or moaA, which are involved in molybdenum cofactor biosynthesis. The spontaneous mutant frequency and induced mutagenic potency of mutagens due to the extended ΔuvrB mutation are due largely to the deletion of uvrB and to some extent of moeA/moaA at the frameshift hisD3052 allele of TA98 but involve other genes in addition to uvrB and moeA/moaA at the base‐substitution hisG46 allele of TA100. The extended ΔuvrB mutation does not prevent the detection of mutagens that would have been detected in a strain containing a single uvrB defect. Because of the deletion of moeA/moaA, the extended uvrB deletion generally enhanced spontaneous and induced mutagenicity, especially at the base‐substitution allele. This enhanced sensitivity may underlay the severe health effects in humans who have mutations in molybdenum cofactor biosynthesis genes. Environ. Mol. Mutagen., 2007. © 2007 Wiley‐Liss, Inc.

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Environmental and Molecular Mutagenesis

Tập 48 Số 8

694-705

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