Ca(2+) current-deficient pawn mutants are promoted to queens during chronic depolarization of Paramecium tetraurelia.
Ca(2+) current-deficient pawn mutants are promoted to queens during chronic depolarization of Paramecium tetraurelia.
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Ca(2) 电流缺陷的 pawn 突变体在草履虫慢性去极化过程中被提升为蚁后。
DOI：
10.1007/s002329900575
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Hammond,JA
中科院分区：
文献类型：
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作者：
Preston,RR;Hammond,JA
慢性KCl诱导的四脲草履虫（Parameciumtetraurelia）去极化可增强其钙依赖性后向游泳行为，持续时间为8-24小时。已经适应20 mmKCl的细胞显示出介导草履虫纤毛逆转（伊卡）的Ca 2+电流特性的几个显著变化，包括电压敏感性的正向偏移和失活的显著减缓。为了解释这些变化，我们研究了慢性去极化对通常不表达Ca 2+电流或向后游泳的突变体的影响。令人惊讶的是，pawn B突变细胞在KCl暴露期间缓慢恢复逆转其纤毛的能力，其时间过程反映了野生型的行为适应。这种行为伴随着一种新的钙电流（IQUEEN）的表达，其电压敏感性相对于野生型钙电流为正，并且缓慢地转变。在适应过程中IQUEEN在野生型中的偶然表达很容易解释观察到的I κ B的变化。我们还研究了慢性去极化对Dancer的影响，Dancer是一种以前认为具有钙激活缺陷的突变体。通过控制细胞外KCl浓度，突变表型可以被抑制或大大放大，这表明Dancer损伤反而导致IQUEEN的不适当调节。
Chronic KCl-induced depolarization ofParamecium tetraureliaenhances Ca2+-dependent backward swimming behavior over a period of 8–24 hr. Here, we investigated the electrophysiological mechanisms underlying this adaptive phenomenon using voltage-clamp techniques. Cells that had been adapted to 20 mmKCl showed several significant changes in the properties of the Ca2+current that mediates ciliary reversal inParamecium(ICa), including a positive shift in voltage sensitivity and a significant slowing of inactivation. In seeking an explanation for these changes, we examined the effects of chronic depolarization on mutants that do not normally express a Ca2+current or swim backward. Surprisingly,pawn Bmutant cells slowly regained the ability to reverse their cilia during KCl exposure with a time course that mirrored behavioral adaptation of the wild type. This behavior was accompanied by expression of a novel Ca2+current (IQUEEN) whose voltage sensitivity was shifted positive with respect to the wild-type Ca2+current and that was slow to inactivate. Coincidental expression ofIQUEENin the wild type during adaptation would readily explain the observed changes inICakinetics. We also examined the effects of chronic depolarization onDancer,a mutant suggested previously to have anICainactivation defect. The mutant phenotype could be suppressed or exaggerated greatly by manipulating extracellular KCl concentration, suggesting thatDancerlesion instead causes inappropriate regulation ofIQUEEN.