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Related Experiment Videos

Carbomycin resistance in mouse L cells.

C L Bunn, J M Eisenstadt

    Somatic Cell Genetics
    |November 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

    A mouse cell mutant resistant to carbomycin was identified. Further experiments indicate this carbomycin resistance is likely controlled by a nuclear gene, not mitochondrial DNA.

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    Area of Science:

    • Cell Biology
    • Genetics
    • Molecular Biology

    Background:

    • Macrolide antibiotics like carbomycin are crucial in research and medicine.
    • Understanding antibiotic resistance mechanisms is vital for developing new therapies.
    • Mitochondrial and nuclear genes play distinct roles in cellular functions, including antibiotic response.

    Purpose of the Study:

    • To investigate the genetic basis of carbomycin resistance in a mouse cell line.
    • To determine whether carbomycin resistance is encoded by nuclear or mitochondrial DNA.
    • To characterize a newly isolated carbomycin-resistant mouse cell mutant.

    Main Methods:

    • Isolation and characterization of a carbomycin-resistant mouse cell line (LM(TK-)).
    • Cell fusion experiments (hybrid and cybrid formation) to assess genetic contribution.

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  • Enucleation and karyoplast-cell fusion techniques to differentiate cytoplasmic inheritance.
  • Assessment of mitochondrial protein synthesis sensitivity to carbomycin and chloramphenicol.

    • Main Results:

    • A stable carbomycin-resistant mutant was isolated from mouse LM(TK-) cells.
    • Mitochondrial protein synthesis in the mutant was carbomycin resistant but chloramphenicol sensitive.
    • Cell fusion experiments showed most hybrids were sensitive to carbomycin, suggesting nuclear control.
    • Cybrid formation and karyoplast-cell fusions failed to transfer carbomycin resistance cytoplasmically.

    Conclusions:

    • Carbomycin resistance in this mouse cell mutant is predominantly determined by nuclear genes.
    • Mitochondrial function is not the primary site of carbomycin resistance in this model.
    • The findings contribute to understanding the genetic basis of antibiotic resistance in mammalian cells.