Tn1 generated mutants in the mercuric ion reductase of the Inc P plasmid, R702.
Physiological, biochemical and genetic aspects of resistance to inorganic mercury compounds were examined in a group of mercury sensitive derivatives generated in the Inc P plasmid, R702, by Tn1 insertion. Strains carrying each of these insertion mutations had no detectable mercuric ion reductase, were more sensitive to mercuric ion than a plasmidless strain, and exhibited inducible uptake of Hg2+. These characteristics indicate that the mutants are altered in the Hg(II) reductase. This hypothesis was supported by complementation and recombination analysis with known point and deletion mutations in the mer operon of the Inc FII plasmid, R100. Such experiments showed that the eight insertions studied had occurred in four distinct regions of the Hg(II) reductase structural gene (merA). Complementation data also demonstrated that the regulatory protein determined by the R702 plasmid has no effect on the expression of the micro-constitutive Hg(II) reductase activity expressed by merR mutants of R100.
D004251:DNA Transposable Elements; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000235:genetics; D005816:Genetic Complementation Test; D008628:Mercury / Q000494:pharmacology*; D009154:Mutation; D010088:Oxidoreductases / Q000235:genetics; D010957:Plasmids; D011995:Recombination, Genetic
D004251:DNA Transposable Elements; D010088:Oxidoreductases; C021551:mercuric reductase; D008628:Mercury