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Human cells lacking mtDNA: repopulation with exogenous mitochondria by complementation.

M P King1, G Attardi

  • 1Division of Biology, California Institute of Technology, Pasadena 91125.

Science (New York, N.Y.)
|October 27, 1989
PubMed
Summary
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Human cells lacking mitochondrial DNA (mtDNA) require uridine and pyruvate for growth. Introducing new mitochondria revealed that both nuclear and mitochondrial genes influence cellular respiration.

Area of Science:

  • Cell Biology
  • Genetics
  • Metabolic Engineering

Background:

  • Mitochondrial DNA (mtDNA) is crucial for cellular respiration.
  • Ethidium bromide can deplete mtDNA, creating cell lines dependent on specific nutrients.
  • Understanding nuclear-mitochondrial interactions is key to cellular function.

Purpose of the Study:

  • To investigate the metabolic requirements of mtDNA-depleted (rho 0) human cell lines.
  • To establish a method for repopulating rho 0 cells with functional mitochondria.
  • To explore the interplay between nuclear and mitochondrial genomes in determining respiratory competence.

Main Methods:

  • Generation of rho 0 human cell lines via long-term ethidium bromide exposure.
  • Utilizing uridine and pyruvate auxotrophy as selectable markers for mitochondrial complementation.

Related Experiment Videos

  • Introducing exogenous mitochondria from various donors into rho 0 cells.
  • Analysis of the respiratory phenotype of resulting transformant cell lines.

    • Main Results:

    • Rho 0 cells demonstrated a strict dependence on uridine and pyruvate for growth due to respiratory chain deficiency.
    • Successful repopulation of rho 0 cells with functional mitochondria was achieved using complementation.
    • Transformant cell lines often displayed unique respiratory phenotypes, differing from both the rho 0 parent and mitochondrial donor.
    • Evidence suggests a significant role for nuclear-mitochondrial genotype interactions in cellular respiratory function.

    Conclusions:

    • Cellular respiration is critically dependent on functional mitochondrial DNA.
    • Metabolic auxotrophy can serve as an effective selection tool for mitochondrial genetic manipulation.
    • Cellular respiratory competence is a complex trait influenced by the coordinated function of both nuclear and mitochondrial genomes.