Presley J F, Draper R K, Brown D T
Cell Research Institute, University of Texas, Austin 78712-7640.
J Virol. 1991 Mar;65(3):1332-9. doi: 10.1128/JVI.65.3.1332-1339.1991.
Mutant V.24.1, a temperature-sensitive derivative of Chinese hamster ovary cells, defines the End4 complementation group of mutants selected for resistance to protein toxins and has defective lysosomes at the restrictive temperature (P. A. Colbaugh, M. Stookey, and R. K. Draper, J. Cell Biol. 108:2211-2219, 1989). We have investigated the biosynthesis of Sindbis virus envelope glycoproteins in V.24.1 cells. When the cells were infected at the restrictive temperature, the envelope glycoproteins E1 and E2 were undetectable on the cell surface and proteolytic processing of the precursor protein pE2 to envelope protein E2 did not occur. Protein retained intracellularly was sensitive to endoglycosidase H and, by immunofluorescence localization, appeared to accumulate in the endoplasmic reticulum. We conclude that the genetic defect in V.24.1 cells impairs the transport of Sindbis virus glycoproteins, apparently at the level of export from the endoplasmic reticulum.
突变体V.24.1是中国仓鼠卵巢细胞的一种温度敏感衍生物，它定义了因对蛋白质毒素具有抗性而被筛选出的End4互补突变体群，并且在限制温度下具有缺陷性溶酶体（P.A.科尔博、M.斯托基和R.K.德雷珀，《细胞生物学杂志》108:2211 - 2219，1989年）。我们研究了辛德毕斯病毒包膜糖蛋白在V.24.1细胞中的生物合成。当细胞在限制温度下被感染时，包膜糖蛋白E1和E2在细胞表面无法检测到，前体蛋白pE2向包膜蛋白E2的蛋白水解加工也未发生。细胞内保留的蛋白质对内切糖苷酶H敏感，并且通过免疫荧光定位，似乎在内质网中积累。我们得出结论，V.24.1细胞中的遗传缺陷损害了辛德毕斯病毒糖蛋白的运输，显然是在内质网输出水平上。
