Role of the galactose transport system in the retention of intracellular galactose in Escherichia coli

Abstract

A galactose transport system with a high affinity for galactose, Rotman's (β-methyl galactoside permease, has been shown to be essential for the internal induction of the galactose operon in galactokinaseless mutants of Escherichia coli. As the result of a second mutation affecting the β-methylgalactoside permease gene, galactokinaseless mutants were found to have lost the internal induction of the galactose operon. Evidence has been previously presented indicating that this double mutant fails to retain galactose which is endogenously generated from uridine diphosphate galactose. Such a failure in the retention mechanism allows the endogenously generated galactose to be lost into the medium and the intracellular level of galactose to drop below the threshold for the induction of the galactose operon. Comparison of the rates of entry and exit of galactose in this double mutant with the rates in the parental strain has revealed that the mutant loses its internally generated galactose, not by an increase in the rate of exit, but by a marked decrease in the rate of entry. These observations are consistent with the view that the recapture of galactose by a highly efficient permease is responsible for the retention of intracellular galactose.