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JBC, Vol. 250, Issue 19, 7593-7601, Oct, 1975
M. H. Saier Jr, B. U. Feucht and M. T. McCaman
Sugars and other energy sources were found to lower intracellular
concentrations of adenosine 3':5'-monophosphate (cyclic AMP) in strains of
Escherichia coli and Salmonella typhimurium which were deficient for cyclic
AMP phosphodiesterase. This effect required the presence of the specific
transport system responsible for entry of that sugar into the cell and
depended on the intracellular catabolic enzymes. Metabolizable sugars were
more effective than nonmetabolizable sugars in reducing cellular cyclic AMP
levels, and this reduction was blocked partially by uncouplers of oxidative
phosphorylation. Electron donors such as lactate and ascorbate plus
phenazine methosulfate reduced internal cyclic AMP levels in bacterial
membrane vesicles which had been preloaded with the cyclic nucleotide.
Uncouplers of oxidative phosphorylation, but not arsenate, blocked the
energy-stimulated loss of intravesicular cyclic AMP. Employing intact
cells, sugars were shown to have two primary effects on cyclic AMP
metabolism: (a) they inhibited net synthesis of the cyclic nucleotide while
promoting its degradation, and (b) they stimulated efflux of cyclic AMP
into the extracellular fluid. While the former effect was elicited by
metabolizable and nonmetabolizable sugars alike, stimulation of cyclic
nucleotide excretion was only observed with metabolizable sugars. The
results suggest that the extrusion of cyclic AMP from the bacterial cell is
energy-dependent and is driven by an energized membrane state.
Regulation of intracellular adenosine cyclic 3':5'-monophosphate levels in Escherichia coli and Salmonella typhimurium. Evidence for energy-dependent excretion of the cyclic nucleotide
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