Gupta R S, Siminovitch L
Somatic Cell Genet. 1980 May;6(3):361-79. doi: 10.1007/BF01542789.
Diphtheria toxin (DT) resistant mutants (Dipr) have been isolated from a number of different Chinese hamster lines. Among mutants affected in protein synthesis (DiprII class), two distinct phenotypes have been identified. In one class, the entire elongation factor-2 (EF-2) activity becomes resistant to DT-catalyzed ADP-ribosylation (DiprIIa class); these mutants behave recessively upon hybridization with sensitive cells. The second kind of protein synthesis mutants contain nearly normal levels of the ADP-ribosylatable EF-2 activity (DiprIIb class). The hybrids the two types of protein synthesis mutants complement each other indicating that mutations in different genes are responsible for them. While the DiprIIa class of mutants are presumably affected in the EF-2, the lesion in DiprIIb mutants seems to have occurred in a yet unidentified protein synthesis factor. Interesting differences are also observed in the characteristics of mutants that presumably are defective in the entry of toxin into cells (DiprI class).
已从多个不同的中国仓鼠品系中分离出抗白喉毒素（DT）的突变体（Dipr）。在蛋白质合成受影响的突变体（DiprII类）中，已鉴定出两种不同的表型。在一类中，整个延伸因子2（EF-2）活性对白喉毒素催化的ADP核糖基化产生抗性（DiprIIa类）；这些突变体与敏感细胞杂交时表现为隐性。第二种蛋白质合成突变体含有接近正常水平的可被ADP核糖基化的EF-2活性（DiprIIb类）。这两种类型的蛋白质合成突变体的杂种相互互补，表明不同基因中的突变是造成它们的原因。虽然DiprIIa类突变体可能在EF-2中受到影响，但DiprIIb突变体中的损伤似乎发生在一个尚未确定的蛋白质合成因子中。在可能在毒素进入细胞方面存在缺陷的突变体（DiprI类）的特征中也观察到有趣的差异。
