Tufaro F, Snider M D, McKnight S L
J Cell Biol. 1987 Aug;105(2):647-57. doi: 10.1083/jcb.105.2.647.
We have isolated a mutant line of mouse L cells, termed gro29, in which the growth of herpes simplex virus (HSV) and vesicular stomatitis virus (VSV) is defective. The block occurs late in the infectious cycle of both viruses. We demonstrate that HSV and VSV enter gro29 cells normally, negotiate the early stages of infection, yet are impaired at a late stage of virus maturation. During VSV infection of the mutant cell line, intracellular transport of its glycoprotein (G protein) is slowed. Pulse-chase experiments showed that oligosaccharide processing is impeded, and immunofluorescence localization revealed an accumulation of G protein in a juxtanuclear region that contains the Golgi complex. We conclude that export of newly made glycoproteins is defective in gro29 cells, and speculate that this defect may reflect a lesion in the glycoprotein transport apparatus.
我们分离出了一种小鼠L细胞的突变株,称为gro29,其中单纯疱疹病毒(HSV)和水疱性口炎病毒(VSV)的生长存在缺陷。这种阻断发生在两种病毒感染周期的后期。我们证明HSV和VSV能正常进入gro29细胞,顺利通过感染的早期阶段,但在病毒成熟的后期受到损害。在突变细胞系感染VSV期间,其糖蛋白(G蛋白)的细胞内运输减慢。脉冲追踪实验表明寡糖加工受到阻碍,免疫荧光定位显示G蛋白在含有高尔基体复合体的近核区域积累。我们得出结论,gro29细胞中新合成糖蛋白的输出存在缺陷,并推测这种缺陷可能反映了糖蛋白运输装置中的损伤。