A muscle cell variant defective in glycosaminoglycan biosynthesis forms nerve-induced but not spontaneous clusters of the acetylcholine receptor and the 43 kDa protein

摘要: Myotubes of the C2 mouse muscle cell line form clusters ACh receptors (AChRs) at apparently random sites along their length when cultured alone, and near nerve-muscle contact cocultured with neurons. We find in aneural cultures that myotubes a variant, S27, which is defective glycosaminoglycan synthesis, express AChR on surface, but do not clusters. S27 cells also 43 kDa protein cluster it. The altered distribution laminin collagen IV surface suggests basal lamina abnormal. Neither addition exogenous proteoglycans or conditioned medium from wild- type cells, nor growth substrates rich elements caused to appear cultures. When primary neurons, however, formed large neurite contact. were coincident patches protein. Prelabeling experiments indicate least some AChRs arise through aggregation. Although Torpedo agrin induces myotubes, it does so cells. Our suggest spontaneous formation depends upon normal synthesis proteoglycans, nerve-induced clustering not. Thus, there be multiple mechanisms for