Cells of Clostridium pusleurimurn grown on glucose lacked enzyme systems specific for sorbi to1 metabolism : the phosphoenolpyruvate (PEP)-dependent phosphotransferase (PTS) and sorbitol-6-phosphate dehydrogenase. These activities were induced by growth on sorbitol, but were partially repressed by glucose. During growth on excess glucose and sorbitol, the sorbitol PTS was absent until the growth rate declined at the onset of stationary phase. Synthesis of at least two PTS proteins, one soluble and one membrane-bound, was repressed in exponentially growing cells. In contrast to the PTS, sorbitol-6-phosphate dehydrogenase was present during the exponential phase.Glucose and methyl a-glucoside inhibited the activity of the sorbitol PTS in permeabilized cells, and this inhibition was competitive at the level of PEP. This implies that in intact cells sorbitol is excluded by glucose, at least in part due to competition between the glucose and sorbitol phosphotransferases for a common pool of phosphate and energy. Exclusion of sorbitol may be an important factor in the repression of sorbitol metabolism by glucose.
Clostridium pasteurianum is capable of fermentative growth on a number of carbohydrate compounds. Several, including glucose, fructose and sorbitol, are accumulated via a phosphoenolpyruvate-dependent phosphotransferase system (PTS), while the uptake of galactose and gluconate is protonmotive-force-dependent. We have examined the utilization of these substrates by cultures of C. pasteurianum growing on carbohydrate mixtures to determine whether the organism displays preferences for one carbon source over the others; such a preference may indicate the operation of specific mechanisms for regulation of carbohydrate metabolism. In most cases the carbohydrates were co-metabolized. Glucose was utilized together with fructose, gluconate and galactose, although galactose appeared to be favoured over glucose. This preference was not due to repression of synthesis of the glucose PTS. On the other hand, glucose prevented induction of the sorbitol PTS, and led to strong inhibition of sorbitol utilization in uninduced cells. Pre-adaptation of cells to growth on sorbitol counteracted the inhibition by glucose resulting in utilization of glucose and sorbitol at approximately equal rates.
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