The traT protein is able to normalize the phenotype of a plasmid-carried permeability mutation of Salmonella typhimurium.
The isolation of different classes of antibiotic-supersensitive outer membrane permeability mutants of Salmonella typhimurium has been described previously (Sukupolvi et al., 1984, Journal of Bacteriology 159, 704-712). One of these, the SS-A mutation, sensitizes the bacteria to gentian violet and to hydrophobic antibiotics. The phenotype of the SS-A mutant was restored to normal when a cloned fragment of the F plasmid, or the R plasmid R6-5, carrying the genes traS, T and D was introduced on a multicopy plasmid. The introduction of a plasmid carrying only the traT gene showed that this gene was sufficient to restore the phenotype. Only clones with functioning traT (irrespective of copy number) restored the normal antibiotic-resistant phenotype in the SS-A mutant. An incompatibility test using a donor strain which carried transposon Tn10 in the 60 MDa plasmid of S. typhimurium and a recipient in which Tn5 was placed close to the SS-A mutation indicated that the SS-A mutation was located in the 60 MDa virulence plasmid (previously called the cryptic plasmid) of S. typhimurium. The introduction of the large virulence plasmid carrying the SS-A mutant allele into wild-type S. typhimurium or Escherichia coli resulted in strains with a phenotype identical to that of the original SS-A mutant.
D001425:Bacterial Outer Membrane Proteins / Q000235:genetics*; D003001:Cloning, Molecular; D029968:Escherichia coli Proteins; D005798:Genes, Bacterial; D009154:Mutation; D010957:Plasmids; D012486:Salmonella typhimurium / Q000235:genetics*
D001425:Bacterial Outer Membrane Proteins; D029968:Escherichia coli Proteins; C036297:TraT protein, E coli