DISRUPTION OF ENDOPLASMIC-RETICULUM TO GOLGI TRANSPORT LEADS TO THE ACCUMULATION OF LARGE AGGREGATES CONTAINING BETA-COP IN PANCREATIC ACINAR-CELLS

When transport between the rough endoplasmic reticulum (ER) and Golgi complex is blocked by Brefeldin A (BFA) treatment or ATP depletion, th e Golgi apparatus and associated transport vesicles undergo a dramatic reorganization. Because recent studies suggest that coat proteins suc h as beta-COP play an important role in the maintenance of the Golgi c omplex, we have used immunocytochemistry to determine the distribution of beta-COP in pancreatic acinar cells (PAC) in which ER to Golgi tra nsport was blocked by BFA treatment or ATP depletion. In controls, bet a-COP was associated with Golgi cisternae and transport vesicles as ex pected. Upon BFA treatment, PAC Golgi cisternae are dismantled and rep laced by clusters of remnant vesicles surrounded by typical ER transit ional elements that are generally assumed to represent the exit site o f vesicular carriers for ER to Golgi transport. In BFA-treated PAC, be ta-COP was concentrated in large (0.5-1.0 mum) aggregates closely asso ciated with remnant Golgi membranes. In addition to typical ER transit ional elements, we detected a new type of transitional element that co nsists of specialized regions of rough ER (RER) with ribosome-free end s that touched or extended into the beta-COP containing aggregates. In ATP-depleted PAC, beta-COP was not detected on Golgi membranes but wa s concentrated in similar large aggregates found on the cis side of th e Golgi stacks. The data indicate that upon arrest of ER to Golgi tran sport by either BFA treatment or energy depletion, beta-COP dissociate s from PAC Golgi membranes and accumulates as large aggregates closely associated with specialized ER elements. The latter may correspond to either the site of entry or exit for vesicles recycling between the G olgi and the RER.