Abstract
The acquisition of high-level resistance to tubercidin (an adenosine analog) in CHO cells occurs in a single step at high frequency (10−3 to 10−4) without mutagenesis. Analysis of a large number of independent mutants by a fluctuation test (Luria and Delbruck, 1943) indicates that they arise independently of the selection medium and all fall into the same complementation group. All mutants tested lack detectable adenosine kinase activity. An analysis of hybrids between mutant and wild-type cells indicates that resistance to tubercidin is a recessive marker which segregates as would be expected if it were a haploid locus in the parental CHO cell. Resistance to tubercidin is not linked to the X chromosome in CHO cells and appears to occur at much lower frequency in primary Chinese hamster cells and other cultured cell lines.
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Rabin, M.S., Gottesman, M.M. High frequency of mutation to tubercidin resistance in CHO cells. Somat Cell Mol Genet 5, 571–583 (1979). https://doi.org/10.1007/BF01542695
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DOI: https://doi.org/10.1007/BF01542695