Wild type cells of <i>Escherichia coli</i> K-12 are unable to grow on glutamate as the sole source of carbon. Glutamate-utilising mutants have been isolated previously and found to exhibit enhanced glutamate transport. Mutations at two loci <i>gltS</i> and <i>gltR</i> and possibly a third <i>gltC</i> were previously shown by other workers to mediate enhanced glutamate permeability. The <i>gltR</i> locus was suggested to be a negative regulatory for the <i>gltS</i> gene. A mutation at the <i>gltS</i> locus, the <i>gltSo</i> mutation increases the activity of a Na⁺-stimulated glutamate transport system GltI. The regulation of the GltI system was investigated by the isolation of MudX gene fusions which abolished Na⁺-stimulated glutamate transport. Two fusions with 'strong' and 'weak' B-galactosidase activities were isolated. These were both found to map at the <i>gltS</i> locus. Subsequent mapping exercises, suggested that the MudX fusions may be located in separate genes. Transcription of the 'strong' fusion was found to be impaired in the presence of the <i>phs</i> mutation. This is a mutation in the <i>rpoA</i> gene which encodes the -subunit of RNA polymerase. Glutamate-utilising suppressor mutants were isolated in both the MudX gene fusion strains. The suppressor mutations were found to map at the <i>gltR</i> locus. This was found to be the map location of a second glutamate transport system GltII. Thus, the <i>gltR</i> locus was found not to be the location of a negative regulator for the <i>gltS</i> gene. The <i>melAB</i> operon encodes the proteins for melibiose transport and utilisation. No regulatory locus has previously been reported for this transport system. The regulation of the <i>melAB</i> operon was investigated by cloning the <i>melAB</i> promoter into an <i>lacZ</i> expression vector. The region upstream from the <i>melAB</i> promoter was subsequently found to encode a trans-acting positive regulatory necessary for <i>melAB</i> expression. Transcription from the <i>melAB</i> promoter was also found to be impaired by the <i>phs</i> mutation. The results presented in this study substantiate previous observations that the <i>phs</i> mutation causes a generalised transcription defect.