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Isolation and preliminary characterization of 9-β-d-arabinofuranosyladenine-resistant mutants of baby hamster cells

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Somatic Cell Genetics

Abstract

A large number of 9-β-d-arabinofuranosyladenine (araA) -resistant mutants of baby hamster kidney cells (BHK 21/Cl3) were isolated. These mutants can be grouped into three mechanistically distinct classes. All the mutants showed cross-resistance to deoxyadenosine (dAdo). The mechanism of resistance to araA and dAdo in the class I mutants can be attributed to a mutation to adenosine kinase (AK) deficiency. The class II mutants have normal levels of AK, adenosine deaminase, and deoxyadenosine kinase. These mutants also show resistance to 1-β-d-arabinofuranosylcytosine (araC), and the mechanism of resistance is probably due to a mutation in the ribonucleotide reductase gene producing an enzyme that has an increased resistance to the inhibition by 9-β-d-arabinofuranosyladenine 5′-triphosphate (araATP) and 2′-deoxyadenosine 5′-triphosphate (dATP). The class III mutants, unlike those of classes I and II, show extreme adenosine (Ado) sensitivity. The Ados/araAr/dAdor phenotypic properties can be attributed to a single mutation. Classes II and III are novel araA-resistant mutants.

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Chan, V.L., Juranka, P. Isolation and preliminary characterization of 9-β-d-arabinofuranosyladenine-resistant mutants of baby hamster cells. Somat Cell Mol Genet 7, 147–160 (1982). https://doi.org/10.1007/BF01567654

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  • DOI: https://doi.org/10.1007/BF01567654

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