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GENERAL ENHANCEMENT OF MUTAGENIC POTENCY OF VARIOUS MUTAGENS DUE TO DELETED GENES IN THE ΔuvrB STRAINS TA 98 AND TA 100 OF SALMONELLA COMPARED WITH STRAINS CONTAINING ONLY A POINT MUTATION IN uvrB
Citation:
SWARTZ, C., N. PARKS, R. M. SCHAAPER, AND D. M. DEMARINI. GENERAL ENHANCEMENT OF MUTAGENIC POTENCY OF VARIOUS MUTAGENS DUE TO DELETED GENES IN THE ΔuvrB STRAINS TA 98 AND TA 100 OF SALMONELLA COMPARED WITH STRAINS CONTAINING ONLY A POINT MUTATION IN uvrB. Presented at The 9th International Conference on Environmental Mutagens, and the 36th Annual Meeting of the Environmental Mutagen Society, San Francisco, CA, September 03 - 08, 2005.
Description:
The two most common strains used in Ames mutagenicity assays, TA98 and TA 100, contain a �uvrB mutation designed to enhance the mutagenicity of compounds, presumably due to the loss of the nucleotide excision repair system. We showed previously that the �uvrB mutations in these strains resulted in the deletion of 47 genes in TA100 and 119 genes in TA98. Studies involving one of us (R.M.S.) in a �uvrB strain of Escherichia coli showed that deletion of molybdenum cofactor biosynthesis genes, which are also deleted in TA98 and TA100 of Salmonella as part of their respective �uvrB mutations, enhanced the mutagenicity of the base analog N6-hydroxylaminopurine (HAP). To explore the consequences of these gene deletions on mutagenesis in TA98 and TA100, we constructed homologues of TA98 and TA100 containing point mutations in uvrB or the molybdenum cofactor biosynthesis genes moeA or moaA. Using the plate-�incorporation assay, we then tested in these strains the following mutagens, which were representative of various chemical classes: MX (a water disinfection byproduct), 1�nitropyrene, HAP, 2-amino-N6-hydroxylaminopurine (AHAP), benzo(a)pyrene, 4�aminobenzene, 2-acetylaminofluorene, and Glu-P-1 (a heterocylic amine food mutagen). Consistent with previous studies in E. coli, HAP and AHAP were base-substitution mutagens and not frameshift mutagens. Their mutagenesis was observed only in strains containing point mutations in both moeA and uvrB and not in strains containing a point mutation in only uvrB. Although AHAP was equally potent (~26,000 rev/�g) in TA100 and a homologue containing a point mutation in both the moeA and uvrB genes, HAP was only ~70% as potent in the homologue as in TA100, inducing 943 and 1179 rev/�g, respectively. Similarly, the remaining chemicals were equally or less mutagenic in strains containing point mutations in both uvrB and moeA compared to TA98 and TA100. Thus, the absence of 47 or 119 genes in TA100 and TA98, respectively, may enhance the mutagenic potency of a variety of mutagens compared to the potency such mutagens might exhibit in strains possessing these genes and having only a point mutation in uvrB.