Hinrichsen R D, Saimi Y, Hennessey T, Kung C
Cell Motil. 1984;4(4):283-95. doi: 10.1002/cm.970040406.
Six mutants of Paramecium tetraurelia, which display altered axonemal responses to Ca++, are described. The mutants, designated atalantas, are impaired in their ability to swim backward when stimulated by ions or heat; instead they spin very rapidly in one place. Three mutants, ataA1-3, are completely unable to swim backward. The three lines, however, can be distinguished from one another by their forward swimming velocities. The remaining three mutants are leaky. ataB swims backward briefly when stimulated, then stops and spins in place. ataC and ataD are extremely leaky and only display the spinning phenotype at elevated temperatures. An electrophysiological analysis reveals that all six mutants have normal membrane properties, including the Ca++ inward current under voltage clamp. When the membrane is disrupted so as to allow the axoneme free access to Ca++, wild-type cells swim backward, but the mutants do not. These data indicate the site(s) of lesion in the mutants is in the axoneme or in some step linking Ca++ influx and the axoneme, not within the ciliary membrane. These mutants may be useful in investigating the role of Ca++ in the regulation of axonemal motion.
本文描述了六种四膜虫（Paramecium tetraurelia）突变体，它们对钙离子（Ca++）的轴丝反应发生了改变。这些被命名为阿塔兰特斯（atalantas）的突变体，在受到离子或热刺激时，向后游动的能力受损；相反，它们会在原地快速旋转。三个突变体ataA1 - 3完全无法向后游动。然而，这三个品系可以通过它们向前游动的速度相互区分。其余三个突变体存在渗漏现象。ataB受到刺激时会短暂地向后游动，然后停止并在原地旋转。ataC和ataD渗漏极为严重，仅在高温下表现出旋转表型。电生理分析表明，所有六个突变体都具有正常的膜特性，包括电压钳制下的钙离子内向电流。当细胞膜被破坏以使轴丝能够自由接触钙离子时，野生型细胞会向后游动，但突变体则不会。这些数据表明，突变体中的损伤位点位于轴丝或钙离子内流与轴丝连接的某些步骤中，而不在纤毛膜内。这些突变体可能有助于研究钙离子在轴丝运动调节中的作用。
