Cytochrome c oxidase-deficient patients have distinct subunit assembly profiles

J Biol Chem. 2001 May 11;276(19):16296-301. doi: 10.1074/jbc.M011162200. Epub 2001 Feb 7.

Abstract

Cytochrome c oxidase (COX) deficiency is the most common respiratory chain defect in childhood and is clinically heterogeneous. We report a study of six patients with COX deficiencies. Two of the patients had as yet undefined defects, three patients had Surf-1 mutations, and one patient had a 15-base pair deletion in the COX III subunit. We show that quantitative measurements of steady-state levels of subunits by monoclonal antibody reactivity, when used in combination with a discontinuous sucrose gradient methods, provide an improved diagnosis of COX deficiencies by distinguishing between kinetic, stability, and assembly defects. The two mutants of undefined etiology had a full complement of subunits with one stable and the other partially unstable to detergent solubilization. Both are likely to carry mutations in nuclear-encoded subunits of the complex. The three Surf-1 mutants and the COX III mutant each had reduced steady-state levels of subunits but variable associations of the residual subunits. This information, as well as aiding in diagnosis, helps in understanding the genotype-phenotype relationships of COX deficiencies and provides insight into the mechanism of assembly of the enzyme complex.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Brain Diseases, Metabolic, Inborn / enzymology
  • Brain Diseases, Metabolic, Inborn / genetics
  • Cell Line
  • Centrifugation, Density Gradient
  • Child, Preschool
  • Cytochrome-c Oxidase Deficiency*
  • Diagnosis, Differential
  • Electron Transport Complex IV / chemistry*
  • Electron Transport Complex IV / genetics
  • Enzyme Stability
  • Fibroblasts / enzymology
  • Humans
  • Infant
  • Kinetics
  • Leigh Disease / diagnosis
  • Leigh Disease / enzymology
  • Leigh Disease / genetics
  • Mitochondrial Myopathies / enzymology
  • Mitochondrial Myopathies / genetics
  • Protein Subunits
  • Sequence Deletion*

Substances

  • Protein Subunits
  • Electron Transport Complex IV