Acetylcholine-activated currents in quail myotubes expressing viral oncogenes

Acetylcholine-activated currents were recorded in cultured myotubes arising from embryonic quail myoblasts transformed by the v-src and v-ras oncogenes. In src-myotubes, the whole cell inward current decayed more slowly than in non-transformed controls. In ras-myotubes, the current had a faster decay and smaller amplitude than in the controls. The single-channel conductance and mean open times recorded from cell-attached patches were similar in transformed and control cells. However, in ras-myotubes the frequency of channel openings strongly decreased with time. It is concluded that oncogenic tyrosine-specific protein kinase (v-src product) and G-like p21 protein (v-ras product) can induce differential changes in the function of nicotinic ACh receptor, perhaps related to specific biochemical events elicited in the establishment of the transformed state.