Ca(2+) current-deficient pawn mutants are promoted to queens during chronic depolarization of Paramecium tetraurelia.

Chronic KCl-induced depolarization of Paramecium tetraurelia enhances Ca(2+)-dependent backward swimming behavior over a period of 8-24 hr. Here, we investigated the electrophysiological mechanisms underlying this adaptive phenomenon using voltage-clamp techniques. Cells that had been adapted to 20 mm KCl showed several significant changes in the properties of the Ca(2+) current that mediates ciliary reversal in Paramecium (I(Ca)), including a positive shift in voltage sensitivity and a significant slowing of inactivation. In seeking an explanation for these changes, we examined the effects of chronic depolarization on mutants that do not normally express a Ca(2+) current or swim backward. Surprisingly, pawn B mutant cells slowly regained the ability to reverse their cilia during KCl exposure with a time course that mirrored behavioral adaptation of the wild type. This behavior was accompanied by expression of a novel Ca(2+) current (I(QUEEN)) whose voltage sensitivity was shifted positive with respect to the wild-type Ca(2+) current and that was slow to inactivate. Coincidental expression of I(QUEEN) in the wild type during adaptation would readily explain the observed changes in I(Ca) kinetics. We also examined the effects of chronic depolarization on Dancer, a mutant suggested previously to have an I(Ca) inactivation defect. The mutant phenotype could be suppressed or exaggerated greatly by manipulating extracellular KCl concentration, suggesting that Dancer lesion instead causes inappropriate regulation of I(QUEEN).