Laboratory of Bacterial Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
PLoS One. 2010 Feb 5;5(2):e9078. doi: 10.1371/journal.pone.0009078.
Retroviral insertional mutagenesis provides an effective forward genetic method for identifying genes involved in essential cellular pathways. A Chinese hamster ovary cell line mutant resistant to several bacterial ADP-ribosylating was obtained by this approach. The toxins used catalyze ADP-ribosylation of eukaryotic elongation factor 2 (eEF-2), block protein synthesis, and cause cell death. Strikingly, in the CHO PR328 mutant cells, the eEF-2 substrate of these ADP-ribosylating toxins was found to be modified, but the cells remained viable. A systematic study of these cells revealed the presence of a structural mutation in one allele of the eEF-2 gene. This mutation, Gly717Arg, is close to His715, the residue that is modified to become diphthamide. This Arg substitution prevents diphthamide biosynthesis at His715, rendering the mutated eEF-2 non-responsive to ADP-ribosylating toxins, while having no apparent effect on protein synthesis. Thus, CHO PR328 cells are heterozygous, having wild type and mutant eEF-2 alleles, with the latter allowing the cells to survive even in the presence of ADP-ribosylating toxins. Here, we report the comprehensive characterization of these cells.
逆转录病毒插入诱变提供了一种有效的正向遗传学方法,可用于鉴定参与重要细胞途径的基因。通过这种方法获得了一种对几种细菌 ADP-核糖基化的抗药性中国仓鼠卵巢细胞系突变体。所使用的毒素催化真核延伸因子 2(eEF-2)的 ADP-核糖基化,阻断蛋白质合成并导致细胞死亡。引人注目的是,在 CHO PR328 突变细胞中,这些 ADP-核糖基化毒素的 eEF-2 底物被发现被修饰,但细胞仍然存活。对这些细胞的系统研究揭示了 eEF-2 基因的一个等位基因中存在结构突变。该突变,甘氨酸 717 到精氨酸 717(Gly717Arg),接近 His715,His715 残基被修饰为二氢叶酸。这种 Arg 取代阻止了 His715 处的二氢叶酸生物合成,使突变的 eEF-2 对 ADP-核糖基化毒素无反应,而对蛋白质合成没有明显影响。因此,CHO PR328 细胞是杂合的,具有野生型和突变型 eEF-2 等位基因,后者允许细胞即使在存在 ADP-核糖基化毒素的情况下也能存活。在这里,我们报告了对这些细胞的全面表征。