ArticleProceedings of the National Academy of Sciences of the United States of America1991
DS28-6, a temperature-sensitive mutant of Chinese hamster ovary cells, expresses key phenotypic changes associated with brefeldin A treatment.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- A fluorescent lipid analogue can be used to monitor secretory activity and for isolation of mammalian secretion mutants.Molecular biology of the cell · 1995Article
- A peripheral protein associated with the cis-Golgi network redistributes in the intermediate compartment upon brefeldin A treatment.The Journal of cell biology · 1994Article
- Disruptions in Golgi structure and membrane traffic in a conditional lethal mammalian cell mutant are corrected by epsilon-COP.The Journal of cell biology · 1994Article
- A brefeldin A-like phenotype is induced by the overexpression of a human ERD-2-like protein, ELP-1.Cell · 1992Article
- Retention of secretory proteins in an intermediate compartment and disappearance of the Golgi complex in an END4 mutant of Chinese hamster ovary cells.The Journal of cell biology · 1992Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
The temperature-sensitive Chinese hamster ovary (CHO) cell mutant DS28-6 has been previously shown to be pleiotropically defective in protein secretion. We have examined the mutant cells to determine the intracellular site of the block in secretion. By transmission electron microscopy a time-dependent disassembly of the Golgi apparatus was found under nonpermissive temperature, which resulted in the loss of the cisternal stack. Complete reorganization of the Golgi apparatus occurred after shift to permissive temperature. Under nonpermissive temperature, a microtubule- and energy-dependent redistribution of Golgi mannosidase II and galactosyltransferase into a pattern characteristic of the endoplasmic reticulum (ER) was observed. Inhibition of protein synthesis by cycloheximide had no influence on Golgi mannosidase II redistribution. Evidence for Golgi apparatus-associated processing of oligosaccharides in the ER was obtained by lectin-gold cytochemistry revealing the presence of the galactose (beta 1----4)N-acetylglucosamine sequence and sialic acid residues. Furthermore, 7-nitrobenz-2-oxa-1,3-diazol-4-yl-tagged ceramide, a lipidic trans-Golgi apparatus marker in CHO cells, exhibited an energy-dependent redistribution into the ER. These effects were fully reversible upon shift to permissive temperature. Thus, mutant DS28-6 cells exhibit key features of the brefeldin A phenotype, which suggests that the observed brefeldin A effects result from interference with a normally occurring cellular process.
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