Identification of Disease-Causing Mutations by Functional Complementation of Patient-Derived Fibroblast Cell Lines

Methods Mol Biol. 2017:1567:391-406. doi: 10.1007/978-1-4939-6824-4_24.

Abstract

Diagnosis of mitochondrial disorders is still hampered by their phenotypic and genotypic heterogeneity. In many cases, exome sequencing, the state-of-the-art method for genetically diagnosing mitochondrial disease patients, does not allow direct identification of the disease-associated gene but rather results in a list of variants in candidate genes. Here, we present a method to validate the disease-causing variant based on functional complementation assays. First, cell lines expressing a wild-type cDNA of the candidate genes are generated by lentiviral infection of patient-derived fibroblasts. Next, oxidative phosphorylation is measured by the Seahorse XF analyzer to assess rescue efficiency.

Keywords: Disease-associated gene; Exome sequencing; Functional complementation; Mitochondrial disorders; Oxygen consumption rate.

MeSH terms

  • Cell Line
  • Fibroblasts / metabolism*
  • Genetic Complementation Test*
  • Genetic Predisposition to Disease*
  • Humans
  • Lentivirus / genetics
  • Mitochondrial Diseases / genetics
  • Mitochondrial Diseases / metabolism
  • Mutation*
  • Oxygen Consumption
  • Plasmids / genetics
  • Statistics as Topic
  • Stress, Physiological
  • Transduction, Genetic