Evidence for a Ca-channel mutation in the K+-resistant mutants ofParamecium

Summary The K⁺-resistant mutants ofParamecium tetraurelia were isolated for their ability to survive high concentrations of K⁺ that kill wild type (Shusterman et al. (1978)Proc. Natl. Acad. Sci. USA755645). These mutants have a normal turnover of the K-analog⁸⁶Rb and do not appear to be defective in their K-regulation. Instead, the following evidence suggests that these mutants have a defective Ca channel that carries a lower-than-normal current: (1) Two K-resistant mutants survive longer than wild type in Ba⁺⁺, which entersParamecium through the Ca channel during an action potential. (2) The most resistant mutant swims backward longer in Ba than wild type and has a much slower uptake of¹³³Ba per second backward swimming. (3) Only the influx of Ba⁺⁺ is altered in this mutant; the efflux of Ba⁺⁺ is normal. All of the phenotypic differences of these mutants, including their lack of adaptation to high K⁺, can be explained by the postulated Ca-channel defect.