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Nuclear inheritance of oligomycin resistance in mouse L cells

Somatic Cell Genetics
|November 1, 1981
PubMed

Insights

Oligomycin resistance in mouse cells was investigated. Results show resistance is inherited through the nucleus, not cytoplasm, suggesting nuclear control of mitochondrial function and DCCD-binding protein genes.

Area of Science:

  • Cell Biology
  • Genetics
  • Biochemistry

Background:

  • Mitochondrial ATPase activity can confer resistance to oligomycin.
  • Mouse L-cell mutants OLI 2, OLI 4, and OLI 14 exhibit oligomycin-resistant mitochondrial ATPase activity.
  • OLI 14 mutant displays additional resistance to DCCD and an altered DCCD-binding protein.

Purpose of the Study:

  • To investigate the inheritance pattern of oligomycin resistance in mouse L-cell mutants.
  • To determine whether oligomycin resistance is maternally (cytoplasmic) or paternally (nuclear) inherited.
  • To elucidate the genetic control of the DCCD-binding protein.

Main Methods:

  • Cell fusion experiments involving enucleated oligomycin-resistant cells and intact sensitive cells.
  • Karyoplast-cell fusions using OLI 14 karyoplasts and sensitive cells.
  • Cell-cell fusions between OLI 14 and sensitive cells.
  • Analysis of mitochondrial ATPase activity to confirm resistance transfer.

Main Results:

  • No transfer of oligomycin resistance was observed through the cytoplasm of OLI 2, OLI 4, or OLI 14 cells.
  • Oligomycin resistance was successfully transferred via karyoplasts of OLI 14 in karyoplast-cell fusions.
  • Oligomycin-resistant hybrids were generated from fusions between OLI 14 and sensitive cells.
  • Transfer of resistance was confirmed at the mitochondrial ATPase level.

Conclusions:

  • Oligomycin resistance in the OLI 14 mutant is primarily under nuclear control.
  • The gene encoding the DCCD-binding protein is likely located in the nucleus of mammalian cells.
  • This suggests nuclear inheritance of mitochondrial traits in mammals.

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