Genetics of a chain-forming mutant ofEscherichia coli: Transduction and dominance of theenvAgene mediating increased penetration to some antibacterial agents

Abstract

SUMMARY: We have recently described a chain-forming mutant ofEscherichia coliwhich showed a decreased resistance to ampicillin and several other antibiotics (Normark, Boman & Mattson, 1969). The gene mediating drug sensitivity was denotedenvAand by conjugation mapped at 2–4 min. Transduction experiments have now shown thatenvAis located betweenleuandaziat 1·5 min. The mapping was facilitated by the finding thatenvAmediated sensitivity to actinomycin D, rifampicin and gentian violet. TheenvAlocus could be genetically differentiated from thepealocus mediating resistance to phenethyl alcohol (Yura & Wada, 1968). Studies using partial diploids revealed thatenvAwas recessive to its wild-type allele both when located on an episome and on the chromosome.Assuming that revertants fromenvAto the wild-type allele could be selected as ampicillin-resistant derivatives, such mutants were isolated and their phenotype characterized. Reversion to ampicillin resistance was accompanied by reversion to insensitivity to actinomycin D. However, not all revertants exhibited wild-type tolerance to rifampicin. Three different ampicillin-resistant revertants were studied genetically. The results indicate that these strains contain suppressor mutations in theenvAregion of the chromosome. It is suggested that theenvAgene, directly or indirectly, affects the EDTA sensitive ‘permeability barrier’ of the surface layer ofEscherichia coli.