Mutant analysis shows that the Ca2+-induced K+ current shuts off one type of excitation in Paramecium.

Abstract

Two mutants of Paramecium tetraurelia, called "pantophobiacs," were found to lack most of the slow Ca2+-induced K+ outward current. Passive properties, the transient Ca2' inward current, and the fast depolarization-induced K+ outward current remain normal. The mutant defect reduces the ability to shut off a normal, excited state of the membrane and results in repeated, long backward swimming instead of the wild-type jerks in response to a variety of ions, to heat, and to touch.Certain mutations are known to affect the nervous system and the behavior of animals (1). In Drosophila (2) and Paramecium (3-7), induced mutations can affect the electric properties of the excitable membranes. Because Paramecium is a large cell and therefore suitable for voltage-clamp experiments, several mutations have been shown to alter the currents through different ion channels (8-11). These mutations have been used as blockers to dissect the pathway of electrogenesis and behavior (4-6, 9, 12-15) and to provide the null controls in the measurements of individual ion currents (14-16) or fluxes (17-19). These mutations also have been used as markers in the search for the gene products involved in the ion-channel functions (20)(21)(22).A paramecium is much like a neuron with several kinds of ion channels differing in their properties and locations. It has at least seven kinds of ion channels with different triggering mechanisms, on-kinetics, off-kinetics, and ion selectivities, some of which are located in the somal membrane and others in the ciliary membrane (23,24). The currents through these channels can be separated by standard physiological methods, by the use of mutants (9,(13)(14)(15), and by deciliation (25,26). The Ca2+-induced K+ current is among the seven kinds of membrane currents studied to date. In paramecia, a step depolarization with a voltage clamp induces a transient Ca2+ inward current, followed by a complex K+ outward current. The Ca2+-induced portion of this complex has been estimated by subtracting the outward current of a pawn mutant, which lacks the Ca2+ current and the Ca2+-induced currents, from the outward current of the wild type. The Ca2+-induced K+ current thus isolated activates slowly, reaching its plateau seconds after depolarization (15

A Drosophila mutation that eliminates a calcium-dependent potassium current.

“…In Paramecium, the only other organism in which comparable mutants are known, the genetic regulation of Ca2"-dependent K+ currents is complex. For example, mutations of at least two different genes eliminate this current (32,33) and mutations of a third gene enhance the current (34). In other organisms, Ca2+-dependent K+ channels are known to be modulated by cAMP-dependent protein kinases (35,36).…”

Slow inactivation of the calcium current of Paramecium is dependent on voltage and not internal calcium.

“…It appeared that in the absence of Ca2+ influx (due to these drugs) the Ca2+ channels are nonetheless inactivated by the K+-induced depolarization, leading to the loss of responsiveness. Saimi, Hinrichsen, Forte & Kung (1983) proposed three types of excitation in free-swimming Paramecium. Type I, lasting several milliseconds, begins with Ca2+ activation and ends by the fast, Ca2+-dependent Ca2+-channel inactivation and K+-delayed rectification.…”

Mutations in genes encoding inner arm dynein heavy chains inTetrahymena thermophila lead to axonemal hypersensitivity to Ca2+

“…Three types of depolarization-induced behaviors have been characterized in ciliates [Saimi et al, 1983]. All three involve ciliary reversal and backward swimming.…”