Frameshift mutagenesis by 9-aminoacridine and ICR191 in Escherichia coli: effects of uvrB, recA and lexA mutations and of plasmid pKM101.
We have studied the effects of different repair capacities on reversion of two Escherichia coli strains (lacZ19124 and lacZ19136) by 9-aminoacridine (9AA) and the acridine half-mustard ICR191. Introduction of a uvrB mutation into these strains led to enhanced ICR191-induced reversion of lacZ19136 and reduced ICR191-induced reversion of lacZ19124. 9AA-induced reversion of lacZ19124 was essentially unchanged while reversion of lacZ19136 was reduced. Plasmid pKM101 reduced reversion of the two markers by each of the mutagens, except in the case of ICR191-induced reversion of the lacZ19124 marker where mutagenesis was slightly enhanced. Mutations in the recA and lexA genes had minimal effects on ICR191- and on 9AA- induced reversion of the lacZ markers; although 9AA-induced reversion of the lacZ19124 marker was somewhat reduced, most of the other results indicated that mutation yields were if anything higher in the recA or lexA backgrounds. Mutagenesis by 9AA and ICR191 would therefore appear to occur independently of the inducible error-prone repair process commonly referred to as SOS repair.[1]References
- Frameshift mutagenesis by 9-aminoacridine and ICR191 in Escherichia coli: effects of uvrB, recA and lexA mutations and of plasmid pKM101. Thomas, S.M., MacPhee, D.G. Mutat. Res. (1985) [Pubmed]
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