Interactions between mutants with defects in two Ca²⁺-dependent K⁺ currents ofParamecium tetraurelia

Summary

Paramecium tetraurelia possesses two Ca²⁺-dependent K⁺ currents, activated upon depolarizationI _K(Ca,d), or upon hyperpolarizationI _K(Ca,h). The two currents are mediated by pharmacologically distinct ion channel populations. Three mutations ofP. tetraurelia affect these current.s Pantophobiac A mutations (pntA) cause calmodulin sequence defects, resulting in the loss of both Ca²⁺-dependent K⁺ currents. A second mutation, TEA-insensitive A (teaA), greatly enhancesI _K(Ca,d) but has no affect onI _K(Ca,h). A third mutation,restless (rst), also increasesI _K(Ca,d) slightly, but its principle effect is in causing an early activation ofI _K(Ca,h). Interactions between the products of these three genes were investigated by constructing three double mutants. BothteaA andrst restoreI _K(Ca,d) andI _K(Ca,h) in pantophobiac A¹, but the phenotypes ofteaA andrst are not corrected by a second mutation. These observations may indicate a role for the gene products ofteaA andrst in regulating the activity ofI _K(Ca,d) andI _K(Ca,h), respectively.