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An explanation of how mutant and wild-type mitochondria might stably co-exist in inherited mitochondrial diseases

Axel Kowald1,2, Felix P Kemeth3, Tom B L Kirkwood1,4

  • 1UK National Innovation Centre for Ageing, The Catalyst, 3 Science Square, Newcastle University, Newcastle upon Tyne NE4 5TG, UK.

PNAS Nexus
|January 30, 2023
PubMed

Insights

Mitochondrial DNA (mtDNA) mutations impact diseases and aging. A new model shows that cells can manage mtDNA mutants, and sometimes, mutant and normal mtDNA can coexist, explaining diverse mitochondrial conditions.

Area of Science:

  • Cellular Biology
  • Genetics
  • Biophysics

Background:

  • Mitochondria are vital organelles in metazoans.
  • Mitochondrial DNA (mtDNA) mutations are linked to diseases and aging.
  • Understanding mtDNA mutant dynamics is crucial.

Purpose of the Study:

  • To model the interplay of mtDNA mutant synthesis and degradation.
  • To investigate the role of mitochondrial dynamics in mtDNA fate.
  • To explore conditions for mutant and wild-type mtDNA coexistence.

Main Methods:

  • Developed a mathematical model incorporating replicative advantage for mtDNA mutants.
  • Included selective degradation influenced by mitochondrial fission and fusion.
  • Analyzed model predictions for mtDNA mutant dynamics.

Main Results:

  • The model demonstrates efficient cellular mechanisms for handling many mtDNA mutant types.
  • Surprisingly, the model predicts stable coexistence of mutant and wild-type mtDNA under specific conditions.
  • This coexistence may explain diverse phenotypes associated with mitochondrial dysfunction.

Conclusions:

  • Cellular processes, including mitochondrial dynamics, play a key role in managing mtDNA mutations.
  • Stable coexistence of mtDNA mutants and wild-type mtDNA is possible, offering new insights.
  • Findings may bridge the understanding between mitochondrial diseases and aging.
Keywords:
agingmathematical modelmitochondrial disease

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