Inhibition of myoblast fusion by the glucosidase inhibitor N-methyl-1-deoxynojirimycin, but not by the mannosidase inhibitor 1-deoxymannojirimycin.
The effects of N-linked-oligosaccharide-processing inhibitors on the fusion of rat L6 myoblasts to form myotubes were examined. The glucosidase inhibitor N-methyl-1-deoxynojirimycin (MDJN) greatly inhibited fusion, whereas the mannosidase inhibitor 1-deoxymannojirimycin (ManDJN) had relatively little effect, although both compounds prevented the formation of N-linked complex oligosaccharides. These results indicate that complex oligosaccharides on glycoproteins do not play a role in myoblast fusion. With MDJN, high-mannose oligosaccharides containing three glucose residues and seven to eight mannose residues were found at the cell surface, whereas with ManDJN, non-glucosylated high-mannose oligosaccharides with seven to nine mannose residues were obtained. These results indicate that the persistence of glucose residues on high-mannose oligosaccharides may be responsible for the inhibition of fusion. It is suggested that glucose either masks the cell-surface recognition process leading to fusion or prevents the cell-surface expression of specific glycoprotein(s) essential to the fusion process.
D017485:1-Deoxynojirimycin / Q000031:analogs & derivatives; D000818:Animals; D002459:Cell Fusion / Q000187:drug effects; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism; D005944:Glucosamine / Q000031:analogs & derivatives* / Q000494:pharmacology; D005959:Glucosidases / Q000037:antagonists & inhibitors*; D006020:Glycopeptides / Q000378:metabolism; D008361:Mannosidases / Q000037:antagonists & inhibitors*; D009132:Muscles / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D009844:Oligosaccharides / Q000378:metabolism; D051381:Rats
D006020:Glycopeptides; D009844:Oligosaccharides; D017485:1-Deoxynojirimycin; D005959:Glucosidases; D008361:Mannosidases; C046090:mannosyl-oligosaccharide 1,2-alpha-mannosidase; D005944:Glucosamine; C033424:N-methyldeoxynojirimycin