Fig. 4.

Intercellular channels formed by CMTX mutations of Cx32 exhibit distinct voltage dependence. Antisense-treated oocytes (see Materials and Methods) were injected with the specified cRNAs and then paired homotypically for measurements of junctional currents, using a dual voltage-clamp procedure.A–E, Time-dependent decay of junctional currents (I_j) induced by transjunctional voltage (V_j) steps of opposite polarity applied in 10 mV increments. Currents from oocytes expressing Cx32wt (A) decayed with a slow time course for V_j ≥ 40 mV. CMTX mutations (B–E) showed changes in voltage-induced channel closure that were particularly pronounced in the case of Del111–116 (D).F–J, Plots describe the relationship ofV_j to steady-state junctional conductance (G_j), normalized to the values obtained at ±10 mV. Smooth lines represent the best fits to Boltzmann equations for which the parameters are given in Table1. G–J, For the sake of comparison,dashed lines show the Boltzmann curve of Cx32wt. Results are shown as the mean ± SEM of the following number of oocyte pairs: Cx32wt, n = 7; L56F, n = 5; E102G, n = 7; Del111–116, n= 6; R220stop, n = 4.