Unique penetrance of hearing loss in a five-generation Chinese family with the mitochondrial 12S rRNA 1555A > G mutation

Acta Otolaryngol. 2011 Sep;131(9):970-5. doi: 10.3109/00016489.2011.575794. Epub 2011 Apr 19.

Abstract

Conclusions: Analysis of the complete mtDNA genome and X-linkage of this five-generation Chinese family revealed that the 1555A > G mutation may lead to deafness.

Objectives: Mutations in mitochondrial DNA (mtDNA) have been found to be associated with sensorineural hearing loss. However, the variable clinical phenotype and incomplete penetrance of mtDNA 1555A > G-induced hearing loss complicate our understanding of this mutation. We aimed to identify whether nuclear genes, mitochondrial haplotypes/variants, and a possible threshold effect are involved in its manifestation in the pedigree.

Methods: We performed clinical, genetic, and X-linkage analysis of a five-generation Chinese family in which all the affected individuals were male.

Results: Clinical evaluation revealed that affected individuals with or without aminoglycoside exposure developed hearing loss extending gradually from 8000 Hz to 4000 Hz and then to 1000 Hz. Using X-linkage analysis and sequencing, we detected an identical homoplasmic 1555A > G mutation in nine individuals, and a previously unreported variant 14163C > T in mtDNA. The new variant 14163C > T coexisted with the 1555A > G mutation in six affected subjects of our pedigree. The previously unreported variant 14163C > T and aminoglycoside exposure may synergize the development of this deafness.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aminoglycosides / toxicity
  • Anti-Bacterial Agents / toxicity
  • Asian People / genetics*
  • Chromosomes, Human, X / genetics*
  • Connexin 26
  • Connexins / genetics
  • DNA Mutational Analysis*
  • DNA, Mitochondrial / genetics*
  • Deafness / chemically induced
  • Deafness / genetics*
  • Female
  • Genes, X-Linked / genetics
  • Genetic Linkage*
  • Genetic Variation / genetics
  • Haplotypes / genetics*
  • Humans
  • Male
  • POU Domain Factors / genetics
  • Pedigree
  • Penetrance*
  • Phenotype
  • Point Mutation / genetics
  • Polymorphism, Genetic / genetics
  • RNA, Ribosomal / genetics*
  • Sex Chromosome Aberrations*

Substances

  • Aminoglycosides
  • Anti-Bacterial Agents
  • Connexins
  • DNA, Mitochondrial
  • POU Domain Factors
  • POU3F4 protein, human
  • RNA, Ribosomal
  • RNA, ribosomal, 12S
  • Connexin 26