The pathway of Golgi cluster formation in okadaic acid-treated cells

J Lucocq, E Berger, C Hug

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


Using stereology and immunoelectron microscopy we examined the pathway of Golgi cluster formation during treatment with the phosphatase inhibitor okadaic acid. During the first hour the Golgi stack of suspension HeLa cells lost 90% of its membrane without appreciable reduction in the number of cisternae. During this time clusters of tubules and vesicles (Golgi clusters) appeared and these contained only a fraction of the Golgi membrane present in untreated cells. Despite the overall reduction in membrane the total amount of immunolabeling for galactosyltransferase over the Golgi clusters of a typical cell was maintained, indicating that galactosyltransferase had been retained in Golgi membranes. The observation that, after 40 min okadaic acid treatment, labeling density for galactosyltransferase within trans Golgi cisternae increased 1.6-fold (n = 3, CE 10%) suggests that membrane loss from trans cisternae was selective. Careful evaluation of immunolabeled clusters showed that most of the galactosyltransferase labeling was located over complex tubular profiles and not vesicular profiles. Tubular structures were also observed during disassembly and these were found both connected to disassembling cisternae and within forming Golgi clusters, indicating that they were intermediates in cluster formation. We also investigated the role of vesicular transport in cluster formation. During disassembly we found no accumulation of COP-coated buds and vesicles over Golgi membrane. However, aluminium fluoride, previously found to arrest transport in the Golgi stack, completely inhibited membrane depletion and stack disassembly. Taken together, our results indicate that during Golgi cluster formation, membrane leaves the Golgi but galactosyltransferase is retained within a tubular reticulum which is a direct descendant of trans-Golgi cisternae. Membrane depletion may require ongoing vesicular transport and we postulate that it arises because of an imbalance in membrane traffic into and out of the Golgi apparatus.
Original languageEnglish
Pages (from-to)318-30
Number of pages13
JournalJournal of Structural Biology
Issue number3
Publication statusPublished - 1995


  • Animals
  • Biological Markers
  • Enzyme Inhibitors
  • Ethers, Cyclic
  • Galactosyltransferases
  • Golgi Apparatus
  • HeLa Cells
  • Humans
  • Interphase
  • Intracellular Membranes
  • Microscopy, Immunoelectron
  • Okadaic Acid
  • Phosphoprotein Phosphatases
  • Rabbits


Dive into the research topics of 'The pathway of Golgi cluster formation in okadaic acid-treated cells'. Together they form a unique fingerprint.

Cite this