ArticleThe Journal of cell biology1997
Dissociation of coatomer from membranes is required for brefeldin A-induced transfer of Golgi enzymes to the endoplasmic reticulum.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 92 citations in OpenAlex.
- Cisternal Maturation of the Golgi Apparatus in Budding Yeast.Sub-cellular biochemistry · 2026Review
- Models of Intracellular Transport: Contradictions and Current Understanding.Sub-cellular biochemistry · 2026Review
- A hollow TFG condensate spatially compartmentalizes the early secretory pathway.Nature communications · 2025Article
- Spatiotemporal dissection of the Golgi apparatus and the ER-Golgi intermediate compartment in budding yeast.eLife · 2024Article
- A reference library for assigning protein subcellular localizations by image-based machine learning.The Journal of cell biology · 2020Article
- Highly conserved motifs within the large Sec7 ARF guanine nucleotide exchange factor GBF1 target it to the Golgi and are critical for GBF1 activity.American journal of physiology. Cell physiology · 2018Article
- COPI-TRAPPII activates Rab18 and regulates its lipid droplet association.The EMBO journal · 2017Article
- Activation of Gαi at the Golgi by GIV/Girdin imposes finiteness in Arf1 signaling.Developmental cell · 2015Article
- An unconventional secretory pathway mediates the cilia targeting of peripherin/rds.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Novel effects of Brefeldin A (BFA) in signaling through the insulin receptor (IR) pathway and regulating FoxO1-mediated transcription.Cellular logistics · 2014Article
- A non-enzymatic function of Golgi glycosyltransferases: mediation of Golgi fragmentation by interaction with non-muscle myosin IIA.Glycobiology · 2013Article
- cis-Golgi proteins accumulate near the ER exit sites and act as the scaffold for Golgi regeneration after brefeldin A treatment in tobacco BY-2 cells.Molecular biology of the cell · 2012Article
- Eeyarestatin 1 interferes with both retrograde and anterograde intracellular trafficking pathways.PloS one · 2011Article
- ADP ribosylation factors 1 and 4 and group VIA phospholipase A₂ regulate morphology and intraorganellar traffic in the endoplasmic reticulum-Golgi intermediate compartment.Molecular biology of the cell · 2010Article
- The secretion inhibitor Exo2 perturbs trafficking of Shiga toxin between endosomes and the trans-Golgi network.The Biochemical journal · 2008Article
- Isoform-selective effects of the depletion of ADP-ribosylation factors 1-5 on membrane traffic.Molecular biology of the cell · 2005Article
- Novel isotypic gamma/zeta subunits reveal three coatomer complexes in mammals.Molecular and cellular biology · 2004Article
- Inhibition of a Golgi complex lysophospholipid acyltransferase induces membrane tubule formation and retrograde trafficking.Molecular biology of the cell · 2003Article
- Exo1: a new chemical inhibitor of the exocytic pathway.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Myosin motors and not actin comets are mediators of the actin-based Golgi-to-endoplasmic reticulum protein transport.Molecular biology of the cell · 2003Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Addition of brefeldin A (BFA) to mammalian cells rapidly results in the removal of coatomer from membranes and subsequent delivery of Golgi enzymes to the endoplasmic reticulum (ER). Microinjected anti-EAGE (intact IgG or Fab-fragments), antibodies against the "EAGE"-peptide of beta-COP, inhibit BFA-induced redistribution of beta-COP in vivo and block transfer of resident proteins of the Golgi complex to the ER; tubulo-vesicular clusters accumulate and Golgi membrane proteins concentrate in cytoplasmic patches containing beta-COP. These patches are devoid of marker proteins of the ER, the intermediate compartment (IC), and do not contain KDEL receptor. Interestingly, relocation of KDEL receptor to the IC, where it colocalizes with ERGIC53 and ts-O45-G, is not inhibited under these conditions. While no stacked Golgi cisternae remain in these injected cells, reassembly of stacks of Golgi cisternae following BFA wash-out is inhibited to only approximately 50%. Mono- or divalent anti-EAGE stabilize binding of coatomer to membranes in vitro, at least as efficiently as GTP(gamma)S. Taken together these results suggest that enhanced binding of coatomer to membranes completely inhibits the BFA-induced retrograde transport of Golgi resident proteins to the ER, probably by inhibiting fusion of Golgi with ER membranes, but does not interfere with the disassembly of the stacked Golgi cisternae and recycling of KDEL receptor to the IC. These results confirm our previous results suggesting that COPI is involved in anterograde membrane transport from the ER/IC to the Golgi complex (Pepperkok et al., 1993), and corroborate that COPI regulates retrograde membrane transport between the Golgi complex and ER in mammalian cells.
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