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Keifer DW, Lucas WJ. Potassium Channels in Chara corallina: CONTROL AND INTERACTION WITH THE ELECTROGENIC H PUMP. Plant Physiol. 1982;69(4):781-8doi: 10.1104/pp.69.4.781.
Keifer, D. W., & Lucas, W. J. (1982). Potassium Channels in Chara corallina: CONTROL AND INTERACTION WITH THE ELECTROGENIC H PUMP. Plant physiology, 69(4), 781-8. https://doi.org/10.1104/pp.69.4.781
Keifer, D W, and Lucas, W J. "Potassium Channels in Chara corallina: CONTROL AND INTERACTION WITH THE ELECTROGENIC H PUMP." Plant physiology vol. 69,4 (1982): 781-8. doi: https://doi.org/10.1104/pp.69.4.781
Keifer DW, Lucas WJ. Potassium Channels in Chara corallina: CONTROL AND INTERACTION WITH THE ELECTROGENIC H PUMP. Plant Physiol. 1982 Apr;69(4):781-8. doi: 10.1104/pp.69.4.781. PMID: 16662296; PMCID: PMC426305.
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Plant Physiol. 1982 Apr;69(4):781-8. doi: 10.1104/pp.69.4.781.

Potassium Channels in Chara corallina: CONTROL AND INTERACTION WITH THE ELECTROGENIC H PUMP.

Plant physiology

D W Keifer, W J Lucas

Affiliations

  1. Department of Botany, University of California at Davis, Davis, California 95616.

PMID: 16662296 PMCID: PMC426305 DOI: 10.1104/pp.69.4.781

Abstract

Plasmalemma electrical properties were used to investigate K(+) transport and its control in internodal cells of Chara corallina Klein ex Willd., em R.D.W. Cell exposure to solutions containing 10 mm KCl caused the potential, normally -250 millivolts (average), to depolarize in two steps. The first step was a 21 millivolt depolarization that lasted from 1 to 40 minutes. The second step started with an action potential and left the membrane potential at -91 millivolts, with a 10-fold reduction in resistance. We suggest that the second step was caused by the opening of K(+) -channels in the membrane. This lowered the resistance and provided a current pathway that partially short-circuited the electrogenic pump. Although largely short-circuited, the electrogenic pump was still operating as indicated by: (a) the depolarized potential of -91 millivolts was more negative than Ek (=-42 millivolts in 10 mm K(+)); (b) a large net K(+) uptake occurred while the cell was depolarized; (c) both the electrogenic pump inhibitor, diethylstilbestrol, and the sulfhydryl-reagent N-ethylmaleimide (which increased the passive membrane permeability) further depolarized the potential in 10 mm KCl.A two-phase recovery back to normal cell potentials occurred upon lowering the K(+) concentration from 10 to 0.2 mm. The first phase was an apparent Nernst potential response to the change in external K(+) concentration. The second phase was a sudden hyperpolarization accompanied by a large increase in membrane resistance. We attribute the second phase to the closing of K(+) -channels and the removal of the associated short-circuiting effect on the electrogenic pump, thereby allowing the membrane to hyperpolarize. Further experiments indicated that the K(+) -channel required Ca(2+) for normal closure, but other ions could substitute, including: Na(+), tetraethylammonium, and 2,4,6-triaminopyrimidine. Apparently, K(+) -channel conductance is determined by competition between Ca(2+) and K(+) for a control (gating?) binding site.

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