Preston R R, Saimi Y, Amberger E, Kung C
Laboratory of Molecular Biology, University of Wisconsin-Madison 53706.
J Membr Biol. 1990 Apr;115(1):61-9. doi: 10.1007/BF01869106.
Paramecium tetraurelia possesses two Ca2(+)-dependent K+ currents, activated upon depolarization IK(Ca,d), or upon hyperpolarization IK(Ca,h). The two currents are mediated by pharmacologically distinct ion channel populations. Three mutations of P. tetraurelia affect these currents. Pantophobiac A mutations (pntA) cause calmodulin sequence defects, resulting in the loss of both Ca2(+)-dependent K+ currents. A second mutation, TEA-insensitive A (teaA), greatly enhances IK(Ca,d) but has no affect on IK(Ca,h). A third mutation, restless (rst), also increases IK(Ca,d) slightly, but its principle effect is in causing an early activation of IK(Ca,h). Interactions between the products of these three genes were investigated by constructing three double mutants. Both teaA and rst restore IK(Ca,d) and IK(Ca,h) in pantophobiac A1, but the phenotypes of teaA and rst are not corrected by a second mutation. These observations may indicate a role for the gene products of teaA and rst in regulating the activity of IK(Ca,d) and IK(Ca,h), respectively.
四膜虫拥有两种Ca2(+)-依赖性K+电流，一种在去极化时被激活，即IK(Ca,d)，另一种在超极化时被激活，即IK(Ca,h)。这两种电流由药理学上不同的离子通道群体介导。四膜虫的三种突变会影响这些电流。泛恐惧症A突变（pntA）会导致钙调蛋白序列缺陷，导致两种Ca2(+)-依赖性K+电流均丧失。第二种突变，即对四乙铵不敏感A（teaA），极大地增强了IK(Ca,d)，但对IK(Ca,h)没有影响。第三种突变，即多动（rst），也会使IK(Ca,d)略有增加，但其主要作用是导致IK(Ca,h)提前激活。通过构建三个双突变体来研究这三个基因产物之间的相互作用。teaA和rst都能恢复泛恐惧症A1中的IK(Ca,d)和IK(Ca,h)，但teaA和rst的表型不会被第二个突变所纠正。这些观察结果可能表明teaA和rst的基因产物分别在调节IK(Ca,d)和IK(Ca,h)的活性中起作用。
