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Abstract
Summary: The acrA mutation in Escherichia coli led to a substantial increase of the acriflavine-binding capacity of the cell, whereas the related mutations acrB (gyrB) and acrC did not. Metal ions such as Na+, K+, Mg2+, Ca2+and Al3+effectively released the bound acriflavine, in proportion to their ionic strengths. The presence of cations, in fact, increased the survival fraction of the cells in the acriflavine-containing medium. Polymyxin B, an antibiotic which binds to membrane phospholipid, competed with acriflavine for binding sites. Cell wall digestion by treatment with lysozyme and EDTA slightly decreased the acriflavine-binding capacity. Almost no difference was observed in acriflavine-binding capacity between intact cells and cells from which lipopolysaccharide has been extracted (46·9% removed from the acrA cells and 47·4% from the acrA +cells). Acriflavine bound to the cells was most effectively extracted by ethanol containing 1% HCl or by 2% (w/v) SDS. The difference in the acriflavine-binding capacity between the acrA and acrA +cells was also observed in the spheroplasts. These facts indicate a relationship between the acrA gene product and the acriflavine-binding capacity of the cells.
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