title: Agonist-induced vesiculation of the Golgi apparatus in pancreatic acinar cells.
abstract: OBJECTIVE
  The pancreatic acinar cell is known to regulate exocytosis, total protein synthesis, and secretory protein transport in response to a secretory stimulus. Whether secretory vesicle formation also is regulated is unclear. In this study, we determined whether agonist stimulation induces morphologic alterations in the acinar cell Golgi apparatus, and we evaluated the role of the vesicle severing protein dynamin.
  
  
  METHODS
  Changes in Golgi structural integrity by examining the distribution of various Golgi and TGN lipid and protein markers in live and fixed cells on stimulation with cholecystokinin were noted in a primary pancreatic acinar cell model. Multiple dynamin reagents were used to examine the distribution and function of this molecular pinchase in resting and stimulated cells.
  
  
  RESULTS
  Regulated secretion in acinar cells induced (1) marked fragmentation of the trans-Golgi network (TGN) that corresponded temporally with an increase in cytoplasmic calcium whereas pre-TGN compartments of the Golgi and regions of the TGN involved in the generation of constitutively trafficking vesicles were unaffected by agonist, and (2) significant recruitment of dynamin to the acinar cell Golgi apparatus that appeared to potentiate fragmentation of the TGN.
  
  
  CONCLUSIONS
  These results suggest that the TGN is a dynamic organelle that fragments in response to cholecystokinin stimulation, a process that may contribute to zymogen granule formation.
authors.affiliation: Center for Basic Research in Digestive Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
authors.forename: Sophie
authors.initials: S
authors.lastname: Dahan
authors.forename: Karen L
authors.initials: KL
authors.lastname: Anderson
authors.forename: Shaun
authors.initials: S
authors.lastname: Weller
authors.forename: Eugene
authors.initials: E
authors.lastname: Krueger
authors.forename: Mark A
authors.initials: MA
authors.lastname: McNiven
mesh_terms: D000818:Animals; D015415:Biomarkers; D002478:Cells, Cultured; D002756:Cholagogues and Choleretics / Q000494:pharmacology*; D034281:Dynamins / Q000378:metabolism; D006056:Golgi Apparatus / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D008055:Lipids / Q000737:chemistry; D046790:Pancreas, Exocrine / Q000166:cytology* / Q000187:drug effects; D051381:Rats; D022142:Secretory Vesicles / Q000378:metabolism / Q000648:ultrastructure; D012844:Sincalide / Q000494:pharmacology*; D021601:trans-Golgi Network / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure
chemical_list: D015415:Biomarkers; D002756:Cholagogues and Choleretics; D008055:Lipids; D034281:Dynamins; D012844:Sincalide