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草履虫线粒体功能控制中的基因相互作用。I. 核基因之间的相互作用

Genetic interactions in the control of mitochondrial functions in Paramecium. I. Interactions between nuclear genes.

作者信息

Ruiz F, Beisson J

出版信息

Mol Gen Genet. 1980;180(3):553-61. doi: 10.1007/BF00268060.

Abstract

The genetic and physiological properties of two nuclear mutants of Paramecium tetraurelia affecting mitochondrial properties, and first screened as resistant to tetrazolium (TTC) are described. The mutant TTC64-1R is strongly deficient in cytochrome c and the mutant TTC66pR is partially deficient in cytochrome aa3; both mutants display cyanide insensitive respiration in exponential growth phase. In the double mutant TTC64-1R -- TTC66pR/TTC64-1R -- TTC66pR the deficiency in cytochrome aa3 due to the TTC66pR mutation is suppressed. The mutation TTC64-1R does not suppress cytochrome aa3 deficiencies due to mitochondrial mutations, but does interact with another nuclear mutation, cl1, (compatible only with mitochondria deficient in cytochrome oxidase) in such a way that the double mutant TTC64-1R -- cl1/TTC64-1R -- cl1 displays a normal amount of cytochrome aa3. The possible mechanisms and physiological significance of these suppressive effects are discussed.

摘要

本文描述了两种影响线粒体特性的四膜虫核突变体的遗传和生理特性,这两种突变体最初是作为对四氮唑(TTC)有抗性而筛选出来的。突变体TTC64 - 1R严重缺乏细胞色素c,突变体TTC66pR部分缺乏细胞色素aa3;在指数生长期,这两种突变体均表现出对氰化物不敏感的呼吸作用。在双突变体TTC64 - 1R -- TTC66pR/TTC64 - 1R -- TTC66pR中,由于TTC66pR突变导致的细胞色素aa3缺乏得到了抑制。TTC64 - 1R突变不会抑制由于线粒体突变导致的细胞色素aa3缺乏,但确实会与另一个核突变cl1相互作用(仅与缺乏细胞色素氧化酶的线粒体相容),使得双突变体TTC64 - 1R -- cl1/TTC64 - 1R -- cl1表现出正常量的细胞色素aa3。文中还讨论了这些抑制作用的可能机制和生理意义。

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