Maternal segmental disomy in Leigh syndrome with cytochrome c oxidase deficiency caused by homozygous SURF1 mutation

Neuropediatrics. 2006 Apr;37(2):88-94. doi: 10.1055/s-2006-924227.

Abstract

Cytochrome c oxidase deficiency (COX) is the most frequent cause of Leigh syndrome (LS), a mitochondrial subacute necrotizing encephalomyelopathy. Most of these LS (COX-) patients show mutations in SURF1 on chromosome 9 (9q34), which encodes a protein essential for the assembly of the COX complex. We describe a family whose first-born boy developed characteristic features of LS. Severe COX deficiency in muscle was caused by a novel homozygous nonsense mutation in SURF1. Segregation analysis of this mutation in the family was incompatible with autosomal recessive inheritance but consistent with a maternal disomy. Haplotype analysis of microsatellite markers confirmed isodisomy involving nearly the complete long arm of chromosome 9 (9q21-9tel). No additional physical abnormalities were present in the boy, suggesting that there are no imprinted genes on the long arm of chromosome 9 which are crucial for developmental processes. This case of segmental isodisomy illustrates that genotyping of parents is crucial for correct genetic counseling.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Child, Preschool
  • Cytochrome-c Oxidase Deficiency / genetics*
  • Female
  • Homozygote
  • Humans
  • Infant
  • Infant, Newborn
  • Leigh Disease / diagnosis
  • Leigh Disease / genetics*
  • Male
  • Membrane Proteins
  • Mitochondrial Proteins
  • Pedigree
  • Pregnancy
  • Prenatal Diagnosis
  • Proteins / genetics*
  • Uniparental Disomy / diagnosis
  • Uniparental Disomy / genetics*

Substances

  • Membrane Proteins
  • Mitochondrial Proteins
  • Proteins
  • Surf-1 protein