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

Paramecium tetraurelia possesses two Ca2+-dependent K+ currents, activated upon depolarizationIK(Ca,d), or upon hyperpolarizationIK(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 enhancesIK(Ca,d) but has no affect onIK(Ca,h). A third mutation,restless (rst), also increasesIK(Ca,d) slightly, but its principle effect is in causing an early activation ofIK(Ca,h). Interactions between the products of these three genes were investigated by constructing three double mutants. BothteaA andrst restoreIK(Ca,d) andIK(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 ofIK(Ca,d) andIK(Ca,h), respectively.