Electrophysiological evidence suggests a defective Ca2+ control mechanism in a new Paramecium mutant.
A new mutant of Paramecium tetraurelia, k-shyA, was characterized behaviorally and electrophysiologically. The mutant cell exhibited prolonged backward swimming episodes in response to depolarizing conditions. Electrophysiological comparison of k-shyA with wild type cells under voltage clamp revealed that the properties of three Ca2+-regulated currents were altered in the mutant. (i) The voltage-dependent Ca2+ current recovered from Ca2+-dependent inactivation two- to 10-fold more slowly than wild type. Ca2+ current amplitudes were also reduced in the mutant, but could be restored by EGTA injection. (ii) The decay of the Ca2+-dependent K+ tail current was slower in the mutant. (iii) The decay of the Ca2+-dependent Na+ tail current was also slower in the mutant. All other membrane properties studied, including the resting membrane potential and resistance and the voltage-sensitive K+ currents, were normal in k-shyA. Considered together, these observations are consistent with a defect in the ability of k-shyA to reduce the free intracellular Ca2+ concentration following stimulation. The possible targets of the genetic lesion and alternative explanations are discussed. The k-shy mutants may provide a useful tool for molecular and physiological analyses of the regulation of Ca2+ metabolism in Paramecium.
D000818:Animals; D002118:Calcium / Q000494:pharmacology / Q000502:physiology*; D004533:Egtazic Acid / Q000494:pharmacology; D004553:Electric Conductivity; D007473:Ion Channels / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D009154:Mutation; D010247:Paramecium / Q000235:genetics / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology
D007473:Ion Channels; D004533:Egtazic Acid; D012964:Sodium; D011188:Potassium; D002118:Calcium