Deletions in the r-determinant mer region of plasmid R100-1 selected for loss of mercury hypersensitivy.
A mutant of plasmid R100-1, which conferred cellular hypersensitivity to Hg2+ because of the insertion of Tn801 (TnA) into the gene determining synthesis of mercuric reductase enzyme, allowed further mutational events to be selected which resulted in either reversion to Hg2+ resistance (characteristic plasmid R100-1) or sensitivity at a level characteristic of plasmidless strains. Restriction endonuclease EcoRI and BamHI analysis showed that reversion to resistance resulted from loss of TnA from the R100-mer:Tn801 plasmid, whereas the change from hypersensitivity to sensitivity to Hg2+ usually resulted from deletion of part or all of Tn801 plus plasmid deoxyribonucleic acid sequences corresponding to the operator-proximal end of the mer operon.
D004251:DNA Transposable Elements; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics; D005816:Genetic Complementation Test; D008628:Mercury / Q000494:pharmacology*; D009154:Mutation; D009876:Operon; D011815:R Factors
D004251:DNA Transposable Elements; D008628:Mercury