Fig 9. Combined loss of cep290 and ahi1 does not exacerbate cone degeneration or rhodopsin trafficking defects.

Panels show immunohistochemical analysis of dorsal retinas from wild-type (top), cep290^fh297/fh297 (middle), and cep290^fh297/fh297;ahi1^+/- mutants (bottom) at 6 months of age stained with (A) PNA (red) and Zpr-1 (green) to label cone photoreceptor; (B) Zpr-3 to label rhodopsin; or (C) GRK1 to label rhodopsin kinase. ROS, rod outer segments; COS, cone outer segments; ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; RGC, retinal ganglion cells. Scale bar: 50 μm. (D) Quantification of cone outer segment density or (E) rhodopsin mislocalization from the indicated genotypes at 6 months of age. See methods section for details on quantification. Removing one allele of ahi1 from a cep290^fh297/fh297 mutant background had no effect on cone degeneration or rhodopsin mislocalization. At least 5 unique fish over at least 2 independent experiments were evaluated. **P < 0.01; *** P < 0.0005; **** P < 0.0001 as determined by a 1-way ANOVA with a Multiple Comparisons test and Tukey corrections. Data represented as means ± s.e.m.