Clinical and diagnostic characteristics of complex III deficiency due to mutations in the BCS1L gene

Am J Med Genet A. 2003 Aug 30;121A(2):126-31. doi: 10.1002/ajmg.a.20171.

Abstract

We investigated two siblings of a Spanish family presenting with congenital lactic acidosis. They had severe failure to thrive, liver dysfunction, and renal tubulopathy. An isolated biochemical complex III deficiency was detected in liver. A search for mutations in the human bc1 synthesis like (BCS1L) gene was undertaken. Direct sequencing revealed a missense mutation R45C and a nonsense mutation R56X, both located in exon 1 of BCS1L. The missense mutation in combination with a loss of function of the second allele is responsible for the isolated complex III deficiency in this family.

Publication types

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

MeSH terms

  • ATPases Associated with Diverse Cellular Activities
  • Codon, Nonsense
  • Electron Transport Complex III / deficiency*
  • Electron Transport Complex III / genetics*
  • Fatal Outcome
  • Female
  • Humans
  • Infant, Newborn
  • Liver / embryology
  • Liver / pathology
  • Male
  • Microscopy, Electron
  • Mutation*
  • Mutation, Missense
  • Sequence Analysis, DNA

Substances

  • BCS1L protein, human
  • Codon, Nonsense
  • ATPases Associated with Diverse Cellular Activities
  • Electron Transport Complex III