Characterization of the Transport of Potassium Ions in the Cyanobacterium Anabaena variabilis KutZ

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Abstract
Interrelationships between potassium-ion transport and transplasmalemma electrical-potential difference (AΨm.) 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, (ΔΨK+=–90 mV; ΔΨm=–70 mV to –75 mV, respectively). Dark pretreatment and low temperature (4°C) reduced internal K+ and depolarized ΔΨm. External pH affected K+ translocation and membrane potential; ΔΨm was hyperpolarized at high external pH; transplasmalemma K+ fluxes and internal K+ concentration were also increased at high pH. The effects of pH upon ΔΨm. coupled with the finding that the membrane potential was relatively insensitive to external K+, suggest that ΔΨm 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 ΔΨm. Carbonylcyanide m-chlorophenylhydrazone decreased K+ fluxes, internal K+ and ΔΨm when added in amounts up to 100 μmol · dm−3. However, ΔΨK+ was always more negative than ΔΨm. Valinomycin up to concentrations of 50 μmol · dm−3 increased transplasmalemma K+ fluxes by up to 300%. while changes in ΔΨm were negligible. Internal K+ was unaffected by valinomycin. N,N′-Dicyclohexylcarbodiimide at concentrations up to 100 μmol · dm-3, reduced K+ flux rates and caused a hyperpolarization of ΔΨm. These observations suggest that ΔΨm 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 dorm (i.e. secondary active transport) is not usually important but may operate when primary active mechanisms are blocked.