Camillo Golgi’s 1898 silver-nitrate staining of Purkinje cells revealed an “internal reticular apparatus” that was dismissed as artefact for forty years. Electron microscopy vindicated him, and the organelle that now bears his name is the cell’s sorting and modification hub: every secreted protein, every membrane protein, every M6P-tagged lysosomal enzyme passes through it. Our new 7-module Golgi course covers its architecture, dynamics, and the diseases (>150 congenital disorders of glycosylation) that trace to its dysfunction.
Seven Modules
- M0 — Discovery & Architecture: Camillo Golgi 1898, cis/medial/trans cisternae, the TGN, mammalian ribbon organisation, golgins and GRASPs.
- M1 — Cisternal Maturation: the vesicular-vs-maturation debate, Glick & Malhotra, 2006 yeast live-imaging proof that cisternae change identity over time.
- M2 — COPI & COPII Vesicles: Schekman 2013 Nobel, Sar1 GTPase and Sec23/24 + Sec13/31, Arf1 and coatomer, the KKXX retrieval motif, KDEL receptor, SNAREs/Rabs/tethers (Rothman/Südhof/Schekman).
- M3 — Glycosylation: N-linked OST at the ER, trimming and elaboration in the Golgi, O-GalNAc mucin-type, blood groups (Landsteiner 1930 Nobel), sialyl-Lewis X and selectins, mannose-6-phosphate lysosomal addressing, furin proprotein convertases.
- M4 — Disassembly in Mitosis: GRASP phosphorylation, CDK1/Plk1 triggers, the “Golgi mitotic checkpoint,” Golgi stress response with TFE3/CREB3, neurodegenerative Golgi fragmentation.
- M5 — Golgi in Disease (CDG): congenital disorders of glycosylation (>150 subtypes), COG complex disorders, I-cell disease (GNPTAB mutations), cancer aberrant glycosylation and metastasis, sialyl-Lewis X in leukocyte trafficking.
- M6 — Unconventional Secretion: FGF2 direct PM translocation, IL-1β via gasdermin pores, autophagy-based secretion, GRASP-driven Golgi-bypass routes.