Characterization of the transport of potassium ions in the cyanobacterium Anabaena variabilis Kütz

Abstract

Interrelationships between potassium-ion transport and transplasmalemma electrical-potential difference (delta psi m) have been investigated in Anabaena variabilis (ATCC 29413) by measuring K+ translocation and membrane potential in parallel. At pH 7.0, 5 mmol . dm-3 external K+, there was a thirtyfold accumulation of K+. The K+ equilibrium potential was lower (more negative) than the measured membrane potential by up to 20 mV, (delta psi K+ = -90 mV; delta psi m = -70 mV to -75 mV, respectively). Dark pretreatment and low temperature (4 degrees C) reduced internal K+ and depolarized delta psi m. External pH affected K+ translocation and membrane potential; delta psi m was hyperpolarized at high external pH; transplasmalemma K+ fluxes and internal K+ concentration were also increased at high pH. The effects of pH upon delta psi m, coupled with the finding that the membrane potential was relatively insensitive to external K+, suggest that delta psi m is unlikely to be due primarily to a diffusion potential of K+, but that the membrane potential is maintained by an electrogenic proton-extrusion mechanism. There was no close (obligate) link between K+ transport and changes in delta psi m. Carbonylcyanide m-chlorophenylhydrazone decreased K+ fluxes, internal K+ and delta psi m when added in amounts up to 100 mumol . dm-3. However, delta psi K+ was always more negative than delta psi m. Valinomycin up to concentrations of 50 mumol . dm-3 increased transplasmalemma K+ fluxes by up to 300%, while changes in delta psi m were negligible. Internal K+ was unaffected by valinomycin. N,N'-Dicyclohexylcarbodiimide at concentrations up to 100 mumol . dm-3, reduced K+ flux rates and caused a hyperpolarization of delta psi m. These observations suggest that delta psi m is primarily due to electron transport reactions at the plasmalemma and that K+ transport is energy-dependent. In the presence of dicyclohexylcarbodiimide, internal K+ redistributed in accordance with the membrane potential, suggesting that passive uniport in response to delta psi m (i.e. secondary active transport) is not usually important but may operate when primary active mechanisms are blocked.