New Mutants of Paramecium Tetraurelia Defective in a Calcium Control Mechanism: Genetic and Behavioral Characterizations

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The k-shy mutants of Paramecium tetraurelia are altered in several Ca(2+)-dependent functions which regulate ciliary motility. The isolation, genetics, and phenotypes of these mutants are described. Of six independent isolates, all contained recessive single-factor mutations and comprise two unlinked loci, ksA and ksB. All k-shy strains showed prolonged backward swimming responses to depolarizing stimuli, but gave infrequent responses to some stimuli. At least four k-shy strains displayed temperature sensitivity. Neither ksA nor ksB was allelic or linked to dancer, a mutation causing weak Ca(2+) current inactivation and prolonged backward swimming. Analysis of ks(+);Dn double mutants revealed synergism between the two mutations. The ksA mutant survived Ba(2+) solutions longer than wild type, but was more sensitive to K(+). Together with previous studies, these results are consistent with a defect in reducing intracellular Ca(2+) causing both prolonged ciliary reversal and reduced Ca(2+) channel activity due to more active Ca(2+)-dependent feedback mechanisms. The integration of the Ca(2+)-dependent stimulatory and inhibitory functions is therefore dependent on ks(+) gene functions. The ksA mutant was rescued by microinjection of wild-type cytoplasm, suggesting a possible behavioral assay for factors related to the ksA(+) gene product.

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