Skip to main content
Log in

A calcium-dependent potassium current is increased by a single-gene mutation inParamecium

  • Articles
  • Published:
The Journal of Membrane Biology Aims and scope Submit manuscript

Summary

The membrane currents of wild typeParamecium tetraurelia and the behavioral mutantteaA were analyzed under voltage clamp. TheteaA mutant was shown to have a greatly increased outward current which was blocked completely by the combined use of internally delivered Cs+ and external TEA+. This, along with previous work (Satow, Y., Kung, C., 1976,J. Exp. Biol. 65:51–63) identified this as a K+ current. It was further found to be a calcium-activated K+ current since this increased outward K+ current cannot be elicited when the internal calcium is buffered with injected EGTA. The mutationpwB, which blocks the inward calcium current, also blocks this increased outward K+ current inteaA. This shows that this mutant current is activated by calcium through the normal depolarization-sensitive calcium channel. While tail current decay kinetic analysis showed that the apparent inactivation rates for this calcium-dependent K+ current are the same for mutant and wild type, theteaA current activates extremely rapidly. It is fully activated within 2 msec. This early activation of such a large outward current causes a characteristic reduction in the amplitude of the action potential of theteaA mutant. TheteaA mutation had no effect on any of the other electrophysiological parameters examined. The phenotype of theteaA mutant is therefore a general decrease in responsiveness to depolarizing stimuli because of a rapidly activating calcium-dependent K+ current which prematurely repolarizes the action potential.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  • Brehm, P., Eckert, R. 1978. Calcium entry leads to inactivation of calcium channels inParamecium.Science 202:1203–1206

    Google Scholar 

  • Chang, S.Y., Kung, C. 1976. Selection and analysis of a mutant lacking behavioral response to tetraethylammonium inParamecium tetraurelia.Genet. Res. 27:97–107

    Google Scholar 

  • Eckert, R., Naitoh, Y., Machemer, H. 1976. Calcium in the bioelectric and motor functions ofParamecium.In: Calcium in Biological Systems. C. J. Duncan, editor. pp. 233–255. Cambridge University Press, New York

    Google Scholar 

  • Elkins, T., Ganetsky, B., Wu, C.-F. 1986. ADrosophila mutant that eliminates a calcium-dependent potassium current.Proc. Natl. Acad. Sci. USA 83:8415–8419

    Google Scholar 

  • Haga, N., Forte, M., Ramanathan, R., Hennessey, T., Takahashi, M., Kung, C. 1984. Characterization and purification of a soluble protein controlling Ca-channel activity inParamecium.Cell 39:71–78

    Google Scholar 

  • Hennessey, T.M., Kung, C. 1984. An anticalmodulin drug, W-7, inhibits the voltage-dependent calcium current inParamecium caudatum.J. Exp. Biol. 110:169–181

    Google Scholar 

  • Hennessey, T.M., Kung, C. 1985. Slow inactivation of the calcium current ofParamecium is dependent on voltage and not internal calcium.J. Physiol. (London) 365:165–179

    Google Scholar 

  • Hinrichsen, R.D., Amberger, E., Saimi, Y., Burgess-Cassler, A., Kung, C. 1985. Genetic analysis of mutants with a reduced Ca2+-dependent K+ current inParamecium tetraurelia.Genetics 111:433–455

    Google Scholar 

  • Hinrichsen, R.D., Burgess-Cassler, A., Chase-Soltvedt, B., Hennessey, T., Kung, C. 1986. Calmodulin restores a defective Ca2+-dependent K+ current in a mutant ofParamecium.Science 232:503–506

    Google Scholar 

  • Hinrichsen, R.D., Saimi, Y. 1984. A mutation that alters properties of the Ca2+ channel inParamecium tetraurelia.J. Physiol. (London) 351:397–410

    Google Scholar 

  • Kung, C., Saimi, Y. 1982. The physiological basis of taxes inParamecium.Annu. Rev. Physiol. 44:519–534

    Google Scholar 

  • Kung, C., Saimi, Y. 1985. Calcium channels ofParamecium: A multidisciplinary study.Curr. Topics Membr. Transp. 23:45–66

    Google Scholar 

  • Lattore, R., Miller, C. 1984. Conduction and selectivity in potassium channels.J. Membrane Biol. 71:11–30

    Google Scholar 

  • Moczydlowski, E., Lattore, R. 1983. Gating kinetics of calciumactivated K+ channels from rat muscle incorporated into planar lipid bilayers.J. Gen. Physiol. 82:511–542

    Google Scholar 

  • Naitoh, Y., Eckert, R. 1974. The control of ciliary activity in protozoa.In: Cilia and Flagella. M.A. Sleigh, editor. pp. 305–352. Academic, London-New York

    Google Scholar 

  • Oertel, D., Schein, S.J., Kung, C. 1977. Separation of membrane currents using aParamecium mutant.Nature (London) 268:120–124

    Google Scholar 

  • Petersen, O.H., Maruyama, Y. 1984. Calcium-activated potassium channels and their role in secretion.Nature (London) 307:693–696

    Google Scholar 

  • Richard, E.A. Hinrichsen, R.D., Kung, C. 1985. A single gene mutation that effects a potassium conductance and resting membrane potential inParamecium.J. Neurogenet. 2:239–252

    Google Scholar 

  • Richard, E.A., Saimi, Y., Kung, C. 1986. A mutation that increases a novel calcium-activated potassium conductance ofParamecium tetraurelia.J. Membrane Biol. 91:173–181

    Google Scholar 

  • Saimi, Y. 1986. Calcium-dependent sodium currents inParamecium: Manipulations and effects of hyper-and depolarization.J. Membrane Biol. 92:227–236

    Google Scholar 

  • Saimi, Y., Hinrichsen, R.D., Forte, M., Kung, C. 1983. Mutant analysis shows that the Ca2+-induced K+ current shuts off one type of excitation inParamecium.Proc. Natl. Acad. Sci. USA 80:5112–5116

    Google Scholar 

  • Saimi, Y., Kung, C. 1980. A Ca-induced Na-current inParamecium.J. Exp. Biol. 88:305–325

    Google Scholar 

  • Salkoff, L. 1983.Drosophila mutants reveal two components of fast outward current.Nature (London) 302:249–251

    Google Scholar 

  • Satow, Y., Kung, C. 1979. A “TEA-insensitive” mutant with increased potassium conductance inParamecium tetraurelia.J. Exp. Biol. 65:51–63

    Google Scholar 

  • Satow, Y., Kung, C. 1979. Voltage-sensitive Ca-channels and the transient inward current inParamecium tetraurelia.J. Exp. Biol. 78:149–161

    Google Scholar 

  • Satow, Y., Kung, C. 1980. Ca2+-induced K+ outward current inParamecium tetraurelia.J. Exp. Biol. 88:293–303

    Google Scholar 

  • Schwartz, W., Passow, H. 1983. Calcium-activated K+ channels in erythrocytes and excitable cells.Annu. Rev. Physiol. 45:359–374

    Google Scholar 

  • Sonneborn, T.M. 1970. Methods inParamecium research.In: Methods Cell Physiol.,4:241–339

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Hennessey, T.M., Kung, C. A calcium-dependent potassium current is increased by a single-gene mutation inParamecium . J. Membrain Biol. 98, 145–155 (1987). https://doi.org/10.1007/BF01872127

Download citation

  • Received:

  • Revised:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01872127

Key Words

Navigation