ATP-linked sodium transport in Streptococcus faecalis. I. The sodium circulation.
Streptococcus faecalis, like other bacteria, expels Na+ and accumulates K+. Sodium movements in several bacterial species have been attributed to secondary antiport of Na+ for H+, energized by the proton-motive force. We find a more complex pattern: a circulation of Na+ across the plasma membrane. One limb is the diffusion of Na+, into the cells or out, by a low affinity pathway in response to gradients of concentration and of electrical potential; Na+ movements are enhanced in metabolizing cells. The other limb is the vectorial extrusion of Na+ by a transport system that requires "ATP" (either ATP itself or a related metabolite), even when Na+ is moving downhill. Cells glycolyzing at alkaline pH in buffer containing excess K+ can expel Na+ against a concentration gradient of 100-fold, even in the presence of reagents that block or short circuit the proton circulation (pH gradient and membrane potential both zero). Evidently, under these conditions "ATP" can serve as the energy donor for a primary sodium pump. However, at acid pH, or in presence of low levels of K+, sodium extrusion requires both "ATP" and the proton-motive force. A mutant is described that retains the leak pathway but lacks the "ATP"-linked transport system.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D001693:Biological Transport, Active / Q000187:drug effects; D002462:Cell Membrane / Q000378:metabolism; D004024:Dicyclohexylcarbodiimide / Q000494:pharmacology; D013293:Enterococcus faecalis / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D009154:Mutation; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D013045:Species Specificity; D014634:Valinomycin / Q000494:pharmacology
D014634:Valinomycin; D004024:Dicyclohexylcarbodiimide; D000255:Adenosine Triphosphate; D012964:Sodium; D011188:Potassium