Disruption of the Golgi apparatus and secretory mechanism in the desmid, Closterium acerosum, by brefeldin A

Abstract

The mucilage-secreting desmid, Closterium acerosum, is sensitive to the secretory inhibiting drug, brefeldin A (BFA). After 5 min of treatment with 5 μg ml -1 of BFA, the Golgi body displays the following alterations: the number of cisternae decreases from 12-15 to 6-7; peripheries of cisternae from the same Golgi body often fuse to yield unique profiles; secretory vesicles still emerge from the Golgi body; the cisternal stack dissociates to form irregular masses in the valleys of cytoplasm created by the lobes of the chloroplast. Fluoresbrite bead labelling shows that mucilage production ceases in cells treated with BFA even after only 5 min of treatment. Immunogold labelling using anti-mucilage antibody reveals that mucilage production still occurs in the Golgi body and associated vesicles. Helix pomatia lectin-gold labelling shows that wall synthesis still occurs in BFA-treated Golgi bodies and wall precursors accumulate in the perforate cisternal/vesicular masses seen in the TGN region of the Golgi stack.