R plasmid-mediated enhancement of mutagenesis in strains of Escherichia coli deficient is known repair functions.
The response to four mutagens (UV radiation, methyl methanesulfonate (MMS), cis-platinum dichlorodiamine (cis-PDD), and a 2-aminopurine (AP)) known to cause different types of DNA damage was investigated in the WP2 strain wild-type for DNA repair and in uvrA-, lexA-, polA-, uvrD- and recL- strains. Each strain was also tested after introduction of either the pKM101 or R648 plasmid. The number of revertants produced by a given mutagen in a given bacterial strain depended in a complex way on: (1) the nature of the mutagen and the type of lesion it created in DNA; (2) the prensence and the nature of defects in the chromosomally determined DNA-repair system; and (3) the presence and the nature of plasmids with mutator effect. The results confirm that plasmids enhance mutagenesis through an error-prone DNA-repair system, which is expressed at different levels for different plasmids. Or, alternatively, different repair mechanisms for different plasmids may exist.
D015075:2-Aminopurine / Q000494:pharmacology; D002945:Cisplatin / Q000494:pharmacology; D004260:DNA Repair; D004269:DNA, Bacterial / Q000528:radiation effects*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D005838:Genotype; D008741:Methyl Methanesulfonate / Q000494:pharmacology; D009154:Mutation; D011815:R Factors; D014466:Ultraviolet Rays
D004269:DNA, Bacterial; D015075:2-Aminopurine; D008741:Methyl Methanesulfonate; D002945:Cisplatin