Colicin Tolerance Induced by Ampicillin or Mutation to Ampicillin Resistance in a Strain of Escherichia coli K-12

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A mutant (G11el) of Escherichia coli selected as being resistant to ampicillin and showing signs of an envelope defect was also found to be tolerant to colicins E2 and E3. The colicin tolerance of G11el could be partially repressed by Mg2+ ions. Transition from tolerance to sensitivity and vice versa by shifting the concentration of Mg2+ in the growth medium required several generations. This indicated that synthesis of new envelope material was needed for transition. Previous physiological results have indicated a change in the envelope lipopolysaccharide (LPS) of G11el. However, chemical analyses revealed no differences in carbohydrate composition between LPS from G11el and its parent strain G11al. Genetic experiments showed that the mutation in G11el is located at about 20 min on the E. coli K-12 chromosome. The mutation was dominant over wild type in partial diploids with the mutation located on the episome. Because colicin tolerance was the most striking phenotypic effect as a result of mutation in the actual locus, this gene will be named tolD until the exact gene product is known. Spheroplasts formed from G11al and G11el by ethylenediaminetetraacetate-lysozyme treatment did not adsorb colicin E2; however, penicillin spheroplasts of G11al and G11el were tolerant to colicin E2. Thus, colicin tolerance can be induced biochemically. It is suggested that colicin tolerance often is a secondary consequence of a change in the cell envelope.

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