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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Hear Res. 2014 Jan 11;0:17–24. doi: 10.1016/j.heares.2014.01.001

Figure 4.

Figure 4

Data acquired from Bth mice crossed onto a Tmc1/Tmc2-deficient background. A, Auditory brainstem responses show the mice were profoundly deaf as early as P30, whereas control mice that expressed wild-type TMC1 had normal hearing thresholds. B, Counts of inner hair cell survival showed significant cell loss in Bth mice relative those that expressed wild-type TMC1. C, Inner hair cells that expressed TMC1 Bth on a Tmc1/Tmc2-deficient background had large whole-cell transduction currents suggesting that Bth is not a loss of function mutation. D, Representative mechanotransduction current–voltage relations are shown for inner hair cells that expressed either wild-type TMC1 (black) or TMC1 Bth (gray). Cells were bathed in 100 mM calcium and reversal potential was estimated from the x-intercept. The data suggest that the Bth point mutation causes a significant reduction in calcium selectivity. Modified from Pan et al. (2013).