Abstract
Abstract Drugs that damage DNA by different mechanisms eliminate an F- lac + plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type ( polA + rec + ). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recB recC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF -dependent recombination exclusively.
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