Correlation between loss of a Mg2+ conductance and an adaptation defect in a mutant of Paramecium tetraurelia.

Paramecium tetraurelia responds to chronic KCl-induced depolarization by swimming backward, but the ciliate recovers within seconds and then undergoes a prolonged adaptation period during which sensitivity to external stimuli is altered radically. We examined the role of Mg2+ in this phenomenon, prompted by finding that mutations in the eccentric-A gene both suppressed a Mg(2+)-specific conductance and prevented adaptation. Adaptation of the wild type proceeded normally when extracellular Mg2+ was varied from 0-20 mM, however, suggesting that channel-mediated Mg2+ fluxes were not involved. In seeking alternative explanations for the eccentric mutant phenotype, we ascertained that there was an osmotic component to adaptation but that K(+)-induced depolarization was the primary stimulus. We also noted that wild-type and eccentric mutant cells depolarized by equivalent amounts in KCl, suggesting that the genetic lesion must lie downstream of membrane-potential change. We also examined whether the adaptation-induced behavioral changes and, indeed, the defect in eccentric might be explained in terms of Mg2+ and Na+ efflux during behavioral testing, but experimental observations failed to support this notion. Finally, we consider the possibility that eccentric gene mutation prevents adaptation by interfering with intracellular free Mg2+ homeostasis in Paramecium.