Chan V L, Guttman S
Mutat Res. 1985 Mar;149(1):141-6. doi: 10.1016/0027-5107(85)90019-3.
9-beta-D-Arabinosyladenine (araA)-resistant mutants of baby hamster kidney (BHK) cells can be classified into 3 classes. In order 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 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. In contrast 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 two 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.
幼年仓鼠肾（BHK）细胞的9-β-D-阿拉伯糖基腺嘌呤（araA）抗性突变体可分为3类。为了更好地理解抗性机制以及各种嘌呤核苷细胞毒性的生化基础，制备并分析了突变体细胞与野生型细胞的细胞杂种。I类araA抗性、腺苷激酶缺陷（AK-）等位基因对野生型araA敏感（AK+）基因呈隐性。编码改变的核糖核苷二磷酸还原酶的II类突变等位基因呈共显性。III类突变体表现出多种表型，araAr/dAdor/腺苷敏感（Ados）以及AK活性改变。III类突变体/野生型杂种细胞中araS10d、ara-16c和ara-19a的araA和dAdo抗性等位基因对野生型等位基因均呈隐性，这与共同的抗性机制一致。相比之下，ara-S10d的Ados等位基因是显性的，而ara-16c和ara-19a的是隐性的。这种差异可能反映了增强的Ado敏感性的两种不同机制，或者表明杂种对Ado的敏感性高度依赖于AK活性水平。
