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粗糙脉孢菌中线粒体基因的功能。

The function of mitochondrial genes in Neurospora crassa.

作者信息

Bertrand H, Szakacs N A, Nargang F E, Zagozeski C A, Collins R A, Harrigan J C

出版信息

Can J Genet Cytol. 1976 Sep;18(3):397-409. doi: 10.1139/g76-049.

Abstract

The 18 extranuclear mutants of Neurospora crassa, without exception, have abnormal mitochondrial respiratory systems. On the basis of genetic, phenotypic and physiological criteria, these mutants are divided into four groups: 1) the cytochrome aa3 and b deficient "poky" variants that are defective in mitochondrial ribosomes assembly, 2) the cytochrome aa3 deficient mutants, [mi-3] and [exn-5], that appear to have genetic lesions affecting a component of a regulatory system controlling cytochrome aa3 synthesis, 3) the cytochrome aa3 and b deficient "stopper" mutants with physiological lesions that probably affect mitochondrial protein synthesis, and 4) cni-3, a mutant that is constitutive for an inducible mitochondrial cyanide-insensitive oxidase in spite of having a normal cytochrome mediated electron-transport system. It is proposed that the mitochondrial genophore not only codes for cellular components that are essential for the formation of the mitochondrial protein synthesizing apparatus, but also for components of a regulatory system that coordinates the expression of nuclear and mitochondrial genes during the biogenesis of the mitochondrial electorn-transport system.

摘要

粗糙脉孢菌的18个核外突变体无一例外都具有异常的线粒体呼吸系统。基于遗传学、表型和生理学标准,这些突变体被分为四组:1)细胞色素aa3和b缺陷的“迟缓型”变体,其线粒体核糖体组装存在缺陷;2)细胞色素aa3缺陷的突变体[mi - 3]和[exn - 5],它们似乎具有影响控制细胞色素aa3合成的调节系统组分的遗传损伤;3)细胞色素aa3和b缺陷的“阻断型”突变体,其生理损伤可能影响线粒体蛋白质合成;4)cni - 3,一个尽管具有正常的细胞色素介导的电子传递系统,但可组成型表达可诱导的线粒体氰化物不敏感氧化酶的突变体。有人提出,线粒体基因载体不仅编码线粒体蛋白质合成装置形成所必需的细胞组分,还编码在线粒体电子传递系统生物发生过程中协调核基因和线粒体基因表达的调节系统的组分。

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