Isolation and preliminary characterization of 9-beta-d-arabinofuranosyladenine-resistant mutants of baby hamster cells.
A large number of 9-beta-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-beta-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-beta-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.
D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D003412:Cricetulus; D003429:Cross Reactions; D003839:Deoxyadenosines / Q000494:pharmacology; D004351:Drug Resistance; D007668:Kidney; D009154:Mutation; D014740:Vidarabine / Q000494:pharmacology*
D003839:Deoxyadenosines; D014740:Vidarabine