A C2 muscle cell variant defective in transport of the acetylcholine receptor to the cell surface.
We have previously reported the isolation of variants of the C2 mouse muscle cell line that express reduced amounts of acetylcholine receptors (AChRs) on their surface (Black, R. A., and Hall, Z. W. (1985) Proc. Natl. Acad. Sci. U.S.A. 82, 124-128). One of the variants, T-, makes an approximately normal amount of the AChR but accumulates most of it in an intracellular pool. This pool is stable and does not serve as precursor for surface AChR. Surface levels of insulin receptor and transferrin receptor are normal in T- cells, and a normal proportion of total hemagglutinin is expressed on the surface after infection of the T- variant with influenza virus. Pulse-chase experiments and kinetic analysis show: 1) that T- cells synthesize a normal amount of the alpha subunit but degrade it much more slowly than do wild-type cells; and 2) that newly synthesized alpha subunit is assembled into the AChR at a normal rate. A small fraction of the assembled AChR in T- cells is transported to the surface with normal kinetics, but most of it remains in an internal pool. This variant may provide an important tool for investigation of the factors that regulate AChR assembly and transport to the surface membrane.