AN INDUCIBLE MECHANISM FOR ACCUMULATION OF MELIBIOSE IN ESCHERICHIA COLI

Abstract

E. coli strains B or ML not previously exposed to melibiose do not permit entry of this sugar into most of the cell; nor do the bacteria permit entry of sucrose, inulin, or sulfate, but they are freely permeable to uracil and thy mine. After exposure to either galactose, melibiose, Me-[beta]-galactoside, or ethyl-[beta] -thiogalactoside, strain ML can concentrate any of these sugars at an internal concentration of at least 20 times the level in the medium. Sugars can be recovered unchanged from the bacteria. Properties of the accumulation mechanism suggest that it is an inducible, enzyme -like system, possibly identical to the recently described galactoside-permease, but not the same as [alpha]-galactosidase or [beta]-galactosidase. Melibiose, Me-[alpha]-galactoside, and galactose induce [beta]-galactosidase, but 5 other [alpha]-galactosides do not. Most of the [alpha]-galactosides tested induce the permease of strain [beta] but not in strain ML. The lag in induction of [beta]-galactosidase by melibiose is attributed to the time required for penetration of the sugar into the bacterial cell. E. coli strain ML grown in the presence of galactose subsequently forms [beta]-galactosidase as rapidly in the absence of galactose as in its presence. This effect is attributed to the slow escape of the accumulated galactose from inside the bacteria.