Literature DB >> 7601652

Quantitative determination of heteroplasmy in Leber's hereditary optic neuropathy by single-strand conformation polymorphism.

Y Mashima1, M Saga, Y Hiida, Y Oguchi, M Wakakura, J Kudoh, N Shimizu.   

Abstract

PURPOSE: The maternal inheritance of Leber's hereditary optic neuropathy (LHON) is caused by defects in the genes of mitochondrial DNA (mtDNA). The most prevalent mtDNA mutation, present in 40% to 90% of families with this disease, is a G to A substitution at nucleotide position 11778. The rapid and accurate quantification of heteroplasmy of this mutation will help determine the relative risk for disease expression.
METHODS: The authors conducted screening tests for heteroplasmy in 44 visually affected patients with the 11778 mutation and 34 unaffected members of 36 Japanese families with LHON using the single-strand conformation polymorphism analysis. This method can detect even a single base difference between the sequences of wild type and mutant DNA strands. The percentage of mutant mtDNA was calculated using an image analyzer.
RESULTS: Single-strand conformation polymorphism analysis allowed the detection of heteroplasmy ranging from 5% to 95%. Five (14%) of the 36 families showed heteroplasmy, and 14 (18%) of the 78 persons tested had heteroplasmy ranging from 10% to 94%. Seven patients with heteroplasmy with visual loss had mutant mtDNA ranging from 62% to 94%.
CONCLUSIONS: Single-strand conformation polymorphism analysis is rapid, efficient, and accurate for detecting point mutations and quantifying heteroplasmy in mtDNA. Individuals with heteroplasmy with less than 60% of mutant mtDNA in circulating leukocytes are probably at lesser risk for developing optic atrophy.

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Year:  1995        PMID: 7601652

Source DB:  PubMed          Journal:  Invest Ophthalmol Vis Sci        ISSN: 0146-0404            Impact factor:   4.799


  7 in total

1.  Leber's hereditary optic neuropathy with 14484 mutation in Central Java, Indonesia.

Authors:  Tomoki Nishioka; Mamoru Tasaki; Augustinus Soemantri; Marbaniati Dyat; J C Susanto; Moedrik Tamam; Bambang Sudarmanto; Takafumi Ishida
Journal:  J Hum Genet       Date:  2003-06-24       Impact factor: 3.172

2.  Multiplex fluorescence-based primer extension method for quantitative mutation analysis of mitochondrial DNA and its diagnostic application for Alzheimer's disease.

Authors:  E Fahy; R Nazarbaghi; M Zomorrodi; C Herrnstadt; W D Parker; R E Davis; S S Ghosh
Journal:  Nucleic Acids Res       Date:  1997-08-01       Impact factor: 16.971

3.  Longitudinal study of a heteroplasmic 3460 Leber hereditary optic neuropathy family by multiplexed primer-extension analysis and nucleotide sequencing.

Authors:  S S Ghosh; E Fahy; I Bodis-Wollner; J Sherman; N Howell
Journal:  Am J Hum Genet       Date:  1996-02       Impact factor: 11.025

4.  Mitochondrial DNA mutations increase in early stage Alzheimer disease and are inconsistent with oxidative damage.

Authors:  Jake G Hoekstra; Michael J Hipp; Thomas J Montine; Scott R Kennedy
Journal:  Ann Neurol       Date:  2016-07-13       Impact factor: 10.422

5.  TaqMan-MGB probe quantitative PCR assays to genotype and quantify three mtDNA mutations of Leber hereditary optic neuropathy.

Authors:  Bingqian Xue; Yang Li; Xin Wang; Rui Li; Xin Zeng; Meihua Yang; Xiaohui Xu; Tingbo Ye; Liming Bao; Yi Huang
Journal:  Sci Rep       Date:  2020-07-23       Impact factor: 4.379

6.  A novel technique based on a PNA hybridization probe and FRET principle for quantification of mutant genotype in fibrous dysplasia/McCune-Albright syndrome.

Authors:  Abdullah Karadag; Mara Riminucci; Paolo Bianco; Natasha Cherman; Sergei A Kuznetsov; Nga Nguyen; Michael T Collins; Pamela G Robey; Larry W Fisher
Journal:  Nucleic Acids Res       Date:  2004-04-19       Impact factor: 16.971

7.  Leber's Hereditary Optic Neuropathy - Reply Letter to the Editor.

Authors:  Cristina Manole; Bogdana Tăbăcaru; Simona Stanca; Horia Tudor Stanca
Journal:  Rom J Ophthalmol       Date:  2020 Jan-Mar
  7 in total

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