Isolation and characterization of magbane, a magnesium-lethal mutant of paramecium.

Isolation and characterization of magbane, a magnesium-lethal mutant of paramecium.
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Magbane(草履虫镁致死突变体)的分离和表征。

DOI:
10.1093/genetics/158.3.1061
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发表时间:
2001
期刊:
影响因子:
3.3
通讯作者:
Preston,RR
Preston,RR
中科院分区:
生物学2区
文献类型:
--
作者:
Hammond,JA;Preston,RR

文献摘要

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由于这些途径存在缺陷的基因突变体的存在,促进了对草履虫中负责膜激发和离子控制的机制的认识。通常根据行为异常或对离子的耐受性来选择此类突变体。尽管可以从表型研究中获得一些见解,但很少有人尝试分离离子敏感菌株。在这里,我们报告了“magbane”的分离,这是一种对 Mg2+ 敏感的离子敏感菌株。野生型在生长减慢并最终被抑制(>40mm)之前可以耐受向培养基中添加≥20mmMgCl2,而mgx突变则在10mm时减慢生长。遗传分析表明,该表型是由以前未曾描述过的隐性单基因突变引起的。我们还注意到,先前已充分描述的突变体(不安定)也对 Mg2+ 高度敏感。该突变体的特点是当细胞外 K+ 浓度降低时,由于 Ca2+ 依赖性 K+ 电流的不适当调节,无法控制膜电位。然而,比较mgx和第一突变体表型表明,两种独立的机制可能导致它们的Mg2+致死性。考虑mgx突变可能对维持低细胞内Mg 2+ 所需的转运蛋白产生不利影响的可能性。
Discerning the mechanisms responsible for membrane excitation and ionic control in Paramecium has been facilitated by the availability of genetic mutants that are defective in these pathways. Such mutants typically are selected on the basis of behavioral anomalies or resistance to ions. There have been few attempts to isolate ion-sensitive strains, despite the insights that might be gained from studies of their phenotypes. Here, we report isolation of “magbane,” an ion-sensitive strain that is susceptible to Mg2+. Whereas the wild type tolerated the addition of ≥20mmMgCl2to the culture medium before growth was slowed and ultimately suppressed (at >40mm),mgxmutation slowed growth at 10mm. Genetic analysis indicated that the phenotype resulted from a recessive single-gene mutation that had not been described previously. We additionally noted that a mutant that was well described previously (restless) is also highly sensitive to Mg2+. This mutant is characterized by an inability to control membrane potential when extracellular K+concentrations are lowered, due to inappropriate regulation of a Ca2+-dependent K+current. However, comparing themgxandrstmutant phenotypes suggested that two independent mechanisms might be responsible for their Mg2+lethality. The possibility thatmgxmutation may adversely affect a transporter that is required for maintaining low intracellular Mg2+is considered.