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Contributor Information

  • Name Payam Gammage
  • Institute Cancer Research UK, Glasgow: The Beatson Institute

Tool Details

  • Tool name: 143B m.8993T>G isogenic mTUNE mT80 Cell Line
  • Alternate names: mTUNE 8, mT8
  • Tool type: Cell Lines
  • Tool sub-type: Continuous
  • Parental cell line: 143B human osteosarcoma (m.8993T>G cybrid)
  • Organism: Human
  • Tissue: Bone
  • Cancer type: Bone; Osteosarcoma
  • Disease: Cancer
  • Model: Tumour line
  • Description: The cellular metabolic environemnt is influenced by relative levels of coexistant mutant and wild-type mitochondrial DNAs (heteorplasmy) in a range of diseases for which mitochondrial dysfunction is a feature. Disease phenotypes may be rescued by returning heteroplasmy towards wild-type levels. To investigate this approach, the team led by Payam Gammage have devised a series of cell lines which stably express stable levels of mutatnt m.8993T>G mtDNA heteroplasmy. Cell lines bearing m.8993T>G heteroplasmy of 80, 45, and 10% are available at These lines are derivatives of the m.8993T cybrid cell developed by Prof Eric Schon, and are of of 143B human osteosarcoma lineage. This is part of a series of three cell line (mTUNE); see Related research tools tab.
  • Research area: Cancer; Metabolism
  • Production details: mTUNE cells were generated by Dr Michal Minczuk’s lab and derive from female human osteosarcoma 143B (RRID: CVCL_2270) cybrid cells (Porteous et al., 1998), after correction of m.8993T>G mutation with mitochondrially-targeted zinc finger nucleases (Gammage et al., 2016a). See Gaude et al., 2018 for further details.
  • Additional notes: This is part of a series of three cell line (mTUNE); see Related Reagents tab.

  • For Research Use Only

Target Details

Application Details


  • Format: Frozen
  • Growth medium: Avoid unnecessary freeze/thaw cycles and keep passage duration to below 2-3 months to avoid heteroplasmy shifts.
  • Shipping conditions: Dry ice


  • Available on request


  •   Genome editing in mitochondria corrects a pathogenic mtDNA mutation in vivo.
  •   Enhanced Manipulation of Human Mitochondrial DNA Heteroplasmy In Vitro Using Tunable mtZFN Technology.
  •   NADH Shuttling Couples Cytosolic Reductive Carboxylation of Glutamine with Glycolysis in Cells with Mitochondrial Dysfunction.
  •   Engineered mtZFNs for Manipulation of Human Mitochondrial DNA Heteroplasmy.
  •   Near-complete elimination of mutant mtDNA by iterative or dynamic dose-controlled treatment with mtZFNs.
  •   Mitochondrially targeted ZFNs for selective degradation of pathogenic mitochondrial genomes bearing large-scale deletions or point mutations.