Moehring T J, Moehring J M
J Bacteriol. 1968 Jul;96(1):61-9. doi: 10.1128/jb.96.1.61-69.1968.
Diphtheria toxin inhibited protein synthesis in intact KB cells. The action of the toxin upon the cell did not result in disaggregation of polyribosomes, or in impairment of their ability to function in protein synthesis. A reduction in single ribosomes and a concomitant increase in polyribosomes did result from the action of toxin. Nascent peptides were not cleaved from polyribosomes by the action of toxin, but treatment of fully intoxicated cells with puromycin resulted in cleavage of these peptides, and caused accelerated polyribosome breakdown. Our data indicated that the toxin must enter the cell to exert its effect. The component or components sensitive to toxin were localized in the 100,000 x g supernatant fraction of cytoplasmic extracts. When extracts from intoxicated cells were treated with nicotinamide, a significant proportion of their capacity to synthesize protein was restored. The specificity of this reaction suggested that nicotinamide adenine dinucleotide is involved in the action of toxin in the intact cell, and that one component inactivated by toxin is soluble transferase II.
白喉毒素抑制完整KB细胞中的蛋白质合成。毒素对细胞的作用不会导致多核糖体解聚，也不会损害其在蛋白质合成中的功能能力。毒素的作用确实导致单核糖体减少，同时多核糖体增加。新生肽不会因毒素的作用而从多核糖体上裂解下来，但用嘌呤霉素处理完全中毒的细胞会导致这些肽的裂解，并加速多核糖体的分解。我们的数据表明，毒素必须进入细胞才能发挥其作用。对毒素敏感的一个或多个成分定位于细胞质提取物的100,000×g上清液部分。当用烟酰胺处理中毒细胞的提取物时，其合成蛋白质的能力有很大一部分得以恢复。这种反应的特异性表明，烟酰胺腺嘌呤二核苷酸参与了毒素在完整细胞中的作用，并且被毒素灭活的一个成分是可溶性转移酶II。
