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Genetics of a chain-forming mutant of Escherichia coli: Transduction and dominance of the envA gene mediating increased penetration to some antibacterial agents

Published online by Cambridge University Press:  14 April 2009

Staffan Normark
Staffan Normark
Affiliation:
Department of Microbiology, University of Umeå, S–901 87 Umeå 6, Sweden
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We have recently described a chain-forming mutant of Escherichia coli which showed a decreased resistance to ampicillin and several other antibiotics (Normark, Boman & Mattson, 1969). The gene mediating drug sensitivity was denoted envA and by conjugation mapped at 2–4 min. Transduction experiments have now shown that envA is located between leu and azi at 1·5 min. The mapping was facilitated by the finding that envA mediated sensitivity to actinomycin D, rifampicin and gentian violet. The envA locus could be genetically differentiated from the pea locus mediating resistance to phenethyl alcohol (Yura & Wada, 1968). Studies using partial diploids revealed that envA was recessive to its wild-type allele both when located on an episome and on the chromosome.

Assuming that revertants from envA to 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 the envA region of the chromosome. It is suggested that the envA gene, directly or indirectly, affects the EDTA sensitive ‘permeability barrier’ of the surface layer of Escherichia coli.

Type
Research Article
Information
Genetics Research , Volume 16 , Issue 1 , August 1970 , pp. 63 - 78
Copyright
Copyright © Cambridge University Press 1970

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