Literature DB >> 10090475

A novel heteroplasmic point mutation in the mitochondrial tRNA(Lys) gene in a sporadic case of mitochondrial encephalomyopathy: de novo mutation and no transmission to the offspring.

M Houshmand1, C Lindberg, A R Moslemi, A Oldfors, E Holme.   

Abstract

We have identified a new mutation in the tRNA(Lys) gene of mtDNA, in a 49-year-old patient with mitochondrial encephalomyopathy. The mutation is a heteroplasmic G-->A transition at position 8328, which affects the anticodon stem loop at a conserved site. The mutation was neither found in 100 controls nor in the maternal relatives of the patient. The level of mutated mtDNA was 57% in muscle, 13% in fibroblasts, and 10% in lymphocytes. Histochemistry of muscle tissue revealed cytochrome c oxidase-deficient fibers with abnormal accumulation of mitochondria. Biochemistry of muscle mitochondria showed slight cytochrome c oxidase deficiency. The mean ratio of mutant mtDNA to normal mtDNA in cytochrome c oxidase-positive muscle fibers was 59%, whereas a mean ratio of 95% was found in cytochrome c oxidase-negative fibers. The difference between cytochrome c oxidase-positive and cytochrome c oxidase-negative fibers was highly significant (P < 0.001). The mutation was not found in muscle or lymphocytes of the mother and daughter of the proband. This is the first report of a de novo point mutation in the tRNA(Lys) gene in an individual expressing disease and the first report of lack of transmission of the mutation to the offspring of a patient expressing a mitochondrial encephalomyopathy caused by a point mutation in mtDNA.

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Year:  1999        PMID: 10090475     DOI: 10.1002/(SICI)1098-1004(1999)13:3<203::AID-HUMU4>3.0.CO;2-3

Source DB:  PubMed          Journal:  Hum Mutat        ISSN: 1059-7794            Impact factor:   4.878


  5 in total

1.  Decreased mitochondrial tRNALys steady-state levels and aminoacylation are associated with the pathogenic G8313A mitochondrial DNA mutation.

Authors:  Sandra R Bacman; David P Atencio; Carlos T Moraes
Journal:  Biochem J       Date:  2003-08-15       Impact factor: 3.857

2.  Transmitochondrial mice as models for primary prevention of diseases caused by mutation in the tRNA(Lys) gene.

Authors:  Akinori Shimizu; Takayuki Mito; Chisato Hayashi; Emi Ogasawara; Ryusuke Koba; Issei Negishi; Keizo Takenaga; Kazuto Nakada; Jun-Ichi Hayashi
Journal:  Proc Natl Acad Sci U S A       Date:  2014-02-07       Impact factor: 11.205

3.  Sporadic myopathy and exercise intolerance associated with the mitochondrial 8328G>A tRNALys mutation.

Authors:  Emma L Blakely; Helen Swalwell; Richard K H Petty; Robert McFarland; Douglass M Turnbull; Robert W Taylor
Journal:  J Neurol       Date:  2007-04-06       Impact factor: 4.849

4.  Noninvasive diagnostics of mitochondrial disorders in isolated lymphocytes with high resolution respirometry.

Authors:  Petr Pecina; Hana Houšťková; Tomáš Mráček; Alena Pecinová; Hana Nůsková; Markéta Tesařová; Hana Hansíková; Jan Janota; Jiří Zeman; Josef Houštěk
Journal:  BBA Clin       Date:  2014-10-01

5.  De novo mtDNA point mutations are common and have a low recurrence risk.

Authors:  Suzanne C E H Sallevelt; Christine E M de Die-Smulders; Alexandra T M Hendrickx; Debby M E I Hellebrekers; Irenaeus F M de Coo; Charlotte L Alston; Charlotte Knowles; Robert W Taylor; Robert McFarland; Hubert J M Smeets
Journal:  J Med Genet       Date:  2016-07-22       Impact factor: 6.318

  5 in total

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