Inherent resistance of HeLa cell derivatives to paromomycin |
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Authors: | Clive L Bunn John I Baron Diane Mitchell |
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Institution: | (1) Department of Biology, University of South Carolina, 29208 Columbia, South Carolina |
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Abstract: | Summary The human tumor-derived cell line HeLa S3 and nuclear and mitochondrial gene mutants derived from it are resistant to the
aminoglycoside antibiotic, paromomycin (PAR). Other carcinoma-derived cells, SV40-transformed cells, and four human diploid
fibroblast cell lines are all sensitive to PAR. Sensitivity is dependent on cell density, and at cell numbers greater than
400/cm2 sensitive cells will proliferate in PAR. The resistance to PAR is inherited in a dominant manner in cell-to-cell fusion hybrids,
but is not transferred in cytoplast-to-cell fusions. PAR resistance is therefore encoded by a nuclear gene(s). Resistance
to PAR is not caused by changes in the response to mitochondrial or cytoplasmic protein synthesis to PAR in vitro. The uptake
of PAR is similar in resistant and sensitive cells, and dimethyl sulfoxide does not render resistant cells more sensitive.
Thus, HeLa cell PAR resistance is unlike previously reported ribosomal mutations and may derive from differences in the intracellular
metabolism of PAR.
This work was supported by National Institutes of Health grant number AG 02664, University of South Carolina Biomedical Research
Support grant number S07 RR7160, and by a grant from the Elsa U. Pardee Foundation, all to C. L. B. |
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Keywords: | HeLa cells human fibroblasts paromomycin antibiotic resistance |
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