Codominant and recessive 9-beta-D-arabinofuranosyladenine-resistant mutations of baby hamster cells
Chan, V.L.; Guttman, S.
Mutation Research 149(1): 141-146
1985
ISSN/ISBN: 0027-5107 PMID: 3974620 Document Number: 254825
9-.beta.-D-Arabinosyladenine (araA)-resistant mutants of baby hamster kidney (BHK) cells can be classified into 3 classes. To gain a better understanding of the mechanism(s) of resistance and the biochemical basis of cytotoxicity of various purine nucleosides, cell hybrids of the mutant and wild-type cells were made and analyzed. The class I araA-resistant, adenosine-kinase-deficient (AK-) allele was shown to be recessive to the wild-type araA-sensitive (AK+) gene. The class II mutant allele, which encodes an altered ribonucleoside diphosphate reductase, was shown to be codominant. The class III mutants show multiple phenotypes, araAr/dAdor/adenosine sensitive (Ados) and alteration in AK activity. The araA- and dAdo-resistant alleles of of araS10d, ara-16c and ara-19a in class III mutant/wild-type hybrid cells are all recessive to the wild-type allele, consistent with a common mechanism of resistance. The Ados allele of ara-S10d is dominant while those of ara-16c and ara-19a are recessive. The difference may be a reflection of 2 distinct mechanisms of enhanced Ado sensitivity or, alternatively, it suggests that the sensitivity of the hybrids to Ado is highly dependent on the level of AK activity.