NONBEHAVIORAL SELECTION FOR PAWNS, MUTANTS OF PARAMECIUM AURELIA WITH DECREASED EXCITABILITY

• Published in: Genetics (Austin) Vol. 84; no. 3; pp. 453 - 468
• Main Author: Schein, Stanley J
• Format: Journal Article
• Language: English
• Published: United States Genetics Soc America 01.11.1976
• Subjects: Animals; Barium - pharmacology; Calcium - physiology; Cell Movement; Chlorpromazine - pharmacology; Drug Resistance; Electric Conductivity; Genes, Recessive; Investigations; Mutation - drug effects; Paramecium - physiology
• DOI: 10.1093/genetics/84.3.453
• ISSN: 0016-6731; 1943-2631

The reversal response in Paramecium aurelia is mediated by calcium which carries the inward current during excitation. Electrophysiological studies indicate that strontium and barium can also carry the inward current. Exposure to high concentrations of barium rapidly paralyzes and later kills wild-type paramecia. Following mutagenesis with nitrosoguanidine, seven mutants which continued to swim in the ;high-barium' solution were selected. All of the mutants show decreased reversal behavior, with phenotypes ranging from extremely non-reversing (;extreme' pawns) to nearly wild-type reversal behavior (;partial' pawns). The mutations fall into three complementation groups, identical to the pwA, pwB, and pwC genes of Kunget al. (1975). All of the pwA and pwB mutants withstand longer exposure to barium, the pwB mutants surviving longer than the pwA mutants. Among mutants of each gene, survival is correlated with loss of reversal behavior. Double mutants (A-B, A-C, B-C), identified in the exautogamous progeny of crosses between ;partial' mutants, exhibited a more extreme non-reversing phenotype than either of their single-mutant (;partial' pawn) parents.---Inability to reverse could be expected from an alteration in the calcium-activated reversal mechanism or in excitation. A normal calcium-activated structure was demonstrated in all pawns by chlorpromazine treatment. In a separate report (Schein, Bennett and Katz 1976) the results of electrophysiological investigations directly demonstrate decreased excitability in all of the mutants, a decrease due to an altered calcium activation. The studies of the genetics, the survival in barium and the electro-physiology of the pawns demonstrate that the pwA and pwB genes have different effects on calcium activation.