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一种控制粗糙脉孢菌中细胞色素aa3产生的调节系统。

A regulatory system controlling the production of cytochrome aa3 in Neurospora crassa.

作者信息

Bertrand H, Collins R A

出版信息

Mol Gen Genet. 1978 Oct 25;166(1):1-13. doi: 10.1007/BF00379723.

DOI:10.1007/BF00379723
PMID:216899
Abstract

The mitochondria of the cyt-2-1, cya-3-16, cya-4-23 and 299-1 nuclear mutants and the [mi-3] and [exn-5] cytoplasmic mutants of Neurospora crassa are deficient in cytochrome aa3, while the cyb-1-1 and cyb-2-1 mutants have mitochondrial b-cytochrome deficiencies. However, the mitochondria from cyb-1-1 cyt-2-1, cyb-1-1 [mi-3] and cyb-2-1 [mi-3] double mutants contain 30% to 50% of the amount of cytochrome aa3 that is present in mitochondria from wild-type; i.e. cyb-1-1 and cyb-2-2 act as suppressors of the cytochrome aa3 deficiency phenotypes that are associated with cyt-2-1 and [mi-3] mutations. The production of cytochrome aa3 can be induced in cyt-2-1 and [mi-3] by growing cells in medium containing antimycin A, an inhibitor of electron transport in the cytochrome bc1 segment of the mitochondrial electrontransport chain. Moreover, the growth of the [mi-3] mutant is strongly stimulated by low concentrations of antimycin A. The induction of cytochrome aa3 by antimycin treatments does not occur in [exn-5], cya-4-23 and 299-1 cells; but does take place in cya-3-16 cells. Although some of the seven constituent polypeptides of cytochrome aa3 are present in mitochondria of [mi-3], the holoenzyme complex is not formed in the mutant. In contrast, the mitochondria of cyb-1-1 [mi-3] and cyb-2-2 [mi-3] double mutants contain a fully assembled cytochrome oxidase complex as well as some unassembled subunit polypeptides. The observations are indicative of the existence of at least two regulatory systems controlling the production of cytochrome aa3. One of the circuits appears to control the basal or "constitutive" production of cytochrome oxidase, the other seems to coordinate the level of cytochrome aa3 with some function of the mitochondrial cytochrome bc1 complex, possibly electron transport.

摘要

粗糙脉孢菌的cyt - 2 - 1、cya - 3 - 16、cya - 4 - 23和299 - 1核突变体以及[mi - 3]和[exn - 5]细胞质突变体的线粒体中细胞色素aa3缺乏,而cyb - 1 - 1和cyb - 2 - 1突变体的线粒体存在b - 细胞色素缺陷。然而,cyb - 1 - 1 cyt - 2 - 1、cyb - 1 - 1 [mi - 3]和cyb - 2 - 1 [mi - 3]双突变体的线粒体中细胞色素aa3的含量是野生型线粒体中细胞色素aa3含量的30%至50%;也就是说,cyb - 1 - 1和cyb - 2 - 2可作为与cyt - 2 - 1和[mi - 3]突变相关的细胞色素aa3缺陷表型的抑制因子。通过在含有抗霉素A(线粒体电子传递链细胞色素bc1区段电子传递的抑制剂)的培养基中培养细胞,可在cyt - 2 - 1和[mi - 3]中诱导细胞色素aa3的产生。此外,低浓度的抗霉素A能强烈刺激[mi - 3]突变体的生长。抗霉素处理对细胞色素aa3的诱导在[exn - 5]、cya - 4 - 23和299 - 1细胞中不发生;但在cya - 3 - 16细胞中会发生。虽然细胞色素aa3的七种组成多肽中的一些存在于[mi - 3]的线粒体中,但该突变体中未形成全酶复合物。相比之下,cyb - 1 - 1 [mi - 3]和cyb - 2 - 2 [mi - 3]双突变体的线粒体含有完全组装好的细胞色素氧化酶复合物以及一些未组装的亚基多肽。这些观察结果表明至少存在两个控制系统来控制细胞色素aa3的产生。其中一个回路似乎控制细胞色素氧化酶的基础或“组成型”产生,另一个似乎将细胞色素aa3的水平与线粒体细胞色素bc1复合物的某些功能(可能是电子传递)协调起来。

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