EFFECT OF INHIBITION OF PROTEIN GLYCOSYLATION ON AUXIN-INDUCED GROWTHAND THE OCCURRENCE OF OSMIOPHILIC PARTICLES IN MAIZE (ZEA-MAYS L) COLEOPTILES

Citation
Hg. Edelmann et al., EFFECT OF INHIBITION OF PROTEIN GLYCOSYLATION ON AUXIN-INDUCED GROWTHAND THE OCCURRENCE OF OSMIOPHILIC PARTICLES IN MAIZE (ZEA-MAYS L) COLEOPTILES, Journal of Experimental Botany, 46(292), 1995, pp. 1745-1752
Citations number
33
Categorie Soggetti
Plant Sciences
ISSN journal
00220957
Volume
46
Issue
292
Year of publication
1995
Pages
1745 - 1752
Database
ISI
SICI code
0022-0957(1995)46:292<1745:EOIOPG>2.0.ZU;2-9
Abstract
The dependence of auxin (IAA)-induced elongation growth on protein gly cosylation was investigated in abraded maize (Zea mays L.) coleoptile segments, employing 2-deoxy-D-glucose (DOG) and tunicamycin (TUM) as i nhibitors of protein glycosylation. TUM had no detectable effect on gr owth at 100 mu g ml(-1). DOG impaired growth at concentrations larger than 1 mM. Total inhibition of growth occurred at a concentration of 2 0 mM. Similar effects were observed with mannose and glucosamine. The effect on wall-synthetic processes in the growth-limiting epidermis wa s analysed by tracer incorporation studies. Within 30 min hemicellulos e and cellulose synthesis, measured as H-3-glucose incorporation, was not affected by DOG, indicating that inhibition of growth is not causa lly related to synthesis of both wall components, In contrast, protein synthesis and secretion into the walls, measured as incorporation of H-3-leucine into the TCA-precipitable protoplasmic and wall-bound prot ein, was rapidly inhibited by DOG. Concomitant with the effect on grow th, DOG as well as mannose inhibited the occurrence of osmiophilic par ticles (OPs) which specifically occur at the growth-limiting epidermis during IAA-induced growth. The results provide evidence that IAA-indu ced wall loosening underlying elongation growth is dependent on O-glyc osylation of proteins and their subsequent secretion into the epiderma l walls. It appears that interference with these processes is responsi ble for inhibition of IAA-induced growth by hexoses acting as anti-glu cose antimetabolites.