Literature DB >> 2545162

Cytochrome c oxidase--deficient myogenic cell lines in mitochondrial myopathy.

H Shimoizumi1, M Y Momoi, S Ohta, Y Kagawa, T Momoi, M Yanagisawa.   

Abstract

In a patient with mitochondrial myopathy, the defect of cytochrome c oxidase activity was restricted to some muscle fibers. To isolate cell lines with or without oxidase activity from a single muscle sample, primary cultured cells were transformed by replication origin-defective simian virus 40, and then cloned. The clones were examined by cytochemical staining for cytochrome c oxidase activity. Eight myogenic clones were completely devoid of activity, while the other myogenic and nonmyogenic clones were not. Deficiency of cytochrome c oxidase was stable in culture for at least a year after serial passaging. The amount of mitochondrial DNA in cytochrome c oxidase-deficient cells was the same as in control cells, and no deletion in the mitochondrial DNA was detected. Protein synthesis in mitochondria of the subunits of cytochrome c oxidase and subunit 6 of the ATP synthase complex was markedly decreased, whereas synthesis of the other subunits encoded by mitochondrial DNA was normal. These cloned cell lines provide an excellent system for clarifying the cause of mitochondrial myopathy and for investigating nuclear-mitochondrial genetic interaction.

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Year:  1989        PMID: 2545162     DOI: 10.1002/ana.410250614

Source DB:  PubMed          Journal:  Ann Neurol        ISSN: 0364-5134            Impact factor:   10.422


  3 in total

1.  The mutant mitochondrial genes in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) were selectively amplified through generations.

Authors:  Y Kobayashi; K Ichihashi; S Ohta; K Nihei; Y Kagawa; M Yanagisawa; M Y Momoi
Journal:  J Inherit Metab Dis       Date:  1992       Impact factor: 4.982

2.  Mitochondrial encephalomyopathies and cytochrome c oxidase deficiency: muscle culture study.

Authors:  I Nonaka; Y Koga; A Kikuchi; Y Goto
Journal:  Acta Neuropathol       Date:  1991       Impact factor: 17.088

3.  Respiration-deficient cells are caused by a single point mutation in the mitochondrial tRNA-Leu (UUR) gene in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS).

Authors:  Y Kobayashi; M Y Momoi; K Tominaga; H Shimoizumi; K Nihei; M Yanagisawa; Y Kagawa; S Ohta
Journal:  Am J Hum Genet       Date:  1991-09       Impact factor: 11.025

  3 in total

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