Venturini S, Monti-Bragadin C
Mutat Res. 1978 Apr;50(1):1-8. doi: 10.1016/0027-5107(78)90054-4.
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.