Figure 3

Genetic mutants resistant to neomycin-induced hair cell death due to impaired mechanotransduction activity are also resistant to cadmium-induced hair cell death. (A)ift88^tz288 mutants, which have previously been shown to have reduced mechanotransduction activity (Kindt et al., 2012; Stawicki et al., 2016), are partially resistant to cadmium-induced hair cell death. (B) Representative images of the IO4 Neuromast in ift88 wild-type siblings (top) and ift88 mutant fish (bottom) following treatment with either 0 (left) or 60 (right) μM cadmium chloride. (C)cc2d2a^w38 mutants, which have previously been shown to have normal mechanotransduction activity (Owens et al., 2008; Stawicki et al., 2016), are not resistant to cadmium-induced hair cell death. (D) Representative images of the IO4 Neuromast in cc2d2a wild-type siblings (top) and cc2d2a mutant fish (bottom) following treatment with either 0 (left) or 60 (right) μM cadmium chloride. Due to reduced hair cell number in ift88 mutants data is normalized to the 0 cadmium chloride control for each treatment group. Data are displayed as mean ± standard deviation. *p < 0.05, ***p < 0.001, ****p < 0.0001 by Two-Way ANOVA and Šídák multiple comparisons test. For the ift88 mutant experiment n = 10 fish for wild-type sibling 15 and 120 μM cadmium chloride and mutant 0, 15, and 30 μM cadmium chloride, n = 9 for wild-type sibling 0 μM cadmium chloride and n = 8 for wild-type sibling 30 and 60 μM cadmium chloride and mutant 60 and 120 μM cadmium chloride. For the cc2d2a experiment n = 10 fish for all groups.