INHIBITION OF GOLGI-APPARATUS FUNCTION BY BREFELDIN-A IN MAIZE COLEOPTILES AND ITS CONSEQUENCES ON AUXIN-MEDIATED GROWTH, CELL-WALL EXTENSIBILITY AND SECRETION OF CELL-WALL PROTEINS

Brefeldin A (BFA), a fungal metabolite causing dysfunction of the Golg i apparatus in plant and animal cells, was used to investigate the rol e of secretory processes at the plasma membrane in auxin-mediated elon gation growth of maize (Zea mays L.) coleoptiles. In abraded coleoptil e segments BFA produced, within less than 30 min, a decrease in the in corporation of [H-3]leucine into tightly bound cell-wall proteins, acc ompanied by an increased incorporation into the intracellular pool of putative cell-wall glycoproteins. Total protein synthesis was not affe cted. Electron micrographs revealed striking morphological changes in dictyosomes (especially vesiculation of trans-cisternae), accumulation of Golgi vesicles and dilation of the endoplasmic reticulum. These ef fects are taken as indication that BFA interferes with the secretion o f cell-wall components. Elongation growth of coleoptile segments in th e presence and absence of auxin was inhibited by 80% in 20 mg.l-1 BFA. If BFA was applied to segments growing in the presence of auxin, maxi mum inhibition was reached after about 30 min, indicating that the gro wth response depends on an uninterrupted supply of a cell-wall or plas ma-membrane component (''wall-loosening factor'') delivered by the sec retory pathway. After its secretion, this factor has a rather short gr owth-effective life time. The inhibition of auxin-mediated growth by B FA was accompanied by an elimination of auxin-induced cell-wall extens ibility and by an inhibition of auxin-induced proton excretion. Fusico ccin-induced proton excretion was similarly affected by BFA. It is con cluded that both the wall-loosening process underlying elongation grow th as well as proton excretion depend on an intact secretory pathway f rom the Golgi apparatus to the cell wall; however, a causal relationsh ip between these processes is not warranted by the data.