Correlation between loss of a Mg2+ conductance and an adaptation defect in a mutant of Paramecium tetraurelia.
Correlation between loss of a Mg2+ conductance and an adaptation defect in a mutant of Paramecium tetraurelia.
复制标题
四尿草草履虫突变体中 Mg2 电导损失与适应缺陷之间的相关性。
DOI：
10.1111/j.1550-7408.1999.tb05127.x
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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：
--
作者：
Preston,RR;Hammond,JA
四尿草履虫通过向后游动来应对慢性 KCI 诱导的去极化，但纤毛虫会在几秒钟内恢复，然后经历一个漫长的适应期，在此期间对外部刺激的敏感性发生根本改变。我们研究了 Mg2- 在这种现象中的作用，发现偏心-A 基因中的突变既抑制了 Mg2+- 特异性电导并阻止了适应。然而，当细胞外 Mg2- 在 0-20 mM 范围内变化时，野生型的适应正常进行，这表明不涉及通道介导的 Mg2+ 通量。在寻找偏心突变表型的替代解释时，我们确定适应存在渗透成分，但 K+ 诱导的去极化是主要刺激。我们还注意到，野生型和偏心突变细胞在 KCI 中以等量去极化，这表明遗传损伤必定位于膜电位变化的下游。我们还研究了适应引起的行为变化以及事实上的非偏心缺陷是否可以用行为测试期间的 Mg2+ 和 Na+ 流出来解释，但实验观察未能支持这一观点。最后，我们考虑了草履虫中偏心基因突变通过干扰细胞内游离 Mg2+ 稳态来阻止适应的可能性。
Paramecium tetraureliaresponds to chronic KCI‐induced depolarization by swimming backward, but the ciliate recovers within seconds and then undergoes a prolonged adaptation period during which sensitivity to external stimuli is altered radically. We examined the role of Mg2‐ in this phenomenon, prompted by finding that mutations in theeccentric‐Agene both suppressed a Mg2+‐ specific conductance and prevented adaptation. Adaptation of the wild type proceeded normally when extracellular Mg2‐ was varied from 0‐20 mM, however, suggesting that channel‐mediated Mg2+ fluxes were not involved. In seeking alternative explanations for theeccentricmutant phenotype, we ascertained that there was an osmotic component to adaptation but that K+‐induced depolarization was the primary stimulus. We also noted that wild‐type andeccentricmutant cells depolarized by equivalent amounts in KCI, suggesting that the genetic lesion must lie downstream of membrane‐potential change. We also examined whether the adaptation‐induced behavioral changes and, indeed, the defect ineccentricmight be explained in terms of Mg2+ and Na+ efflux during behavioral testing, but experimental observations failed to support this notion. Finally, we consider the possibility thateccentricgene mutation prevents adaptation by interfering with intracellular free Mg2+ homeostasis inParamecium.