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pubmed:abstractText |
A mutant (ML 308-22) was isolated from Escherichia coli ML 308, which had lost the normal capacity to accumulate lactose analogs despite an increase in the membrane carrier activity. The exit of thiomethylgalactoside was much faster than normal, accounting for the inability of the cell to maintain high intracellular concentrations of galactosides. Growth of the mutant on lactose was normal at high concentrations of sugar and impaired at low concentrations. This transport defect appeared to be limited to the lactose transport system as D-fucose and alpha-aminoisobutyric acid uptake and accumulation were normal. It is inferred from the data that the mutant possessed a defect in the coupling of metabolic energy to lactose transport.
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