Genetic control of inducer exclusion by Escherichia coli

There are two main ways in which enteric bacteria take up carbohydrates from their external media. In ‘group translocation’, the uptake of a number of sugars is coupled to the transfer to them of phosphate from phosphoenolpyruvate (PEP) and the sugars thus appear inside the cells as the phosphate esters. The multi-component phosphotransferase system (PTS) that brings this about was discovered by S. Roseman et al. [ 1 ] ; its properties have been extensively reviewed [ 2,3]. ‘Active transport’, on the other hand, is a term applied to the energy-linked uptake of other sugars, in which no obligatory phosphate transfer occurs and in which the sugar present externally appears, chemically unchanged, as such inside the cells. This process is intimately associated with the flow of electrons through membrane carriers and may be energized by the collapse of proton and/or electrical gradients [4,5] . Sugars that are taken up by Escherichia coli or Salmonella typhimurium via phosphotransferase-mediated ‘group translocation’ include glucose and fructose; they are designated W-sugars’ for convenience. Carbohydrates that are taken up by these bacteria via ‘active transport’ include lactose, maltose, pentoses, gluconate and hexose phosphates; they can be similarly grouped under the term ‘non-PT-sugars’ [3,6] . It would be expected from this distinction that mutants impaired in a sugar-specific component of the PEP-phosphotransferase system would not grow on the appropriate PT-sugar or, if the lesion were in a common component of that system, on any PT-sugar, but that such mutants would-grow on non-PT sugars. However, many mutants of Enzyme I of the PTS @ts Z) have been described which fail to grow both on PT-sugars