Defective transport of Sindbis virus glycoproteins in End4 mutant Chinese hamster ovary cells.
AUTOR(ES)
Presley, J F
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=239909Documentos Relacionados
- Isolation of a Chinese hamster ovary cell mutant defective in intramitochondrial transport of phosphatidylserine
- Internalization of ricin in Chinese hamster ovary cells.
- Selection of mutant Chinese hamster ovary cells altered glycoproteins by means of tritiated fucose suicide.
- A cowpox virus gene required for multiplication in Chinese hamster ovary cells.
- Isolation and partial characterization of a cholesterol-requiring mutant of Chinese hamster ovary cells.