Abstract
A mutant clone of murine S49 cells, DTB6, was isolated in a single step from mutagenized wild type cells by virtue of its resistance to 1 mM thymidine and 1mM dibutyryl cyclic AMP. In comparative growth rate experiments, DTB6 cells were considerably less sensitive than parental cells to the growth inhibitory effects of thymidine and thymidine analogs, but surprisingly were equally sensitive to dibutyryl cyclic AMP. Conversely, DTB6 cells were much more sensitive to the cytotoxic effects of either adenine or adenosine-EHNA. This supersensitivity of DTB6 cells to growth inhibition by adenine could be ameliorated by the addition of hypoxanthine to the culture medium. The complex growth phenotype of the mutant cells could be attributed to a 60% deficiency in AMP deaminase activity and a complete absence of thymidine kinase activity in the mutant cells. Revertants of DTB6 cells possessed wild type levels of AMP deaminase activity but remained deficient in thymidine kinase activity, while another revertant of DTB6 cells expressed 11% of the wild type thymidine kinase level but did not perceptibly change its AMP deaminase activity. The ability to isolate single step mutants with two seemingly independent biochemical abnormalities raises the speculation that there may be some link between cellular functions responsible for purine nucleotide and thymidine metabolism.
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Hanson, S., Ullman, B. 47 AMP DEAMINASE AND THYMIDINE KINASE DEFICIENCIES IN A CLONALLY ISOLATED DERIVATIVE OF MOUSE S49 CELLS. Pediatr Res 24, 119 (1988). https://doi.org/10.1203/00006450-198807000-00071
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DOI: https://doi.org/10.1203/00006450-198807000-00071