Fin and skeletal abnormalities observed in adult ahr2^hu3335 zebrafish.

A–B) Brightfield and (C–D) microCt imaging of adult ahr2⁺ and ahr2^hu3335zebrafish. Notable differences were observed in the dentate (d), premaxilla (pm), maxilla (mx), supraorbital (so), infraorbital 3(inf) and operculum (op).

ahr2^hu3335 embryos are resistant to TCDD-induced developmental abnormalities.

A) Percent of embryos with axis malformations and B) percent incidence pericardial edema at 120 hpf in embryos treated with 0, 0.1, 1 or 10 nM TCDD from 6–24 hpf. Vehicle control groups (c, 0.1% DMSO) are displayed at 10^-4 for graphing purposes. Data represent three independent experiments with 20 embryos per treatment group. C) Representative image of 120 hpf ahr2⁺ and (D) ahr2^hu3335 embryos developmentally exposed to 10 nM TCDD.

CYP1A protein expression patterns are ligand- and AHR isoform-dependent.

CYP1A expression at 120 hpf in (A) ahr2⁺ and (B) ahr2^hu3335 larvae following exposure to 1 nM TCDD from 6–24 hpf. C) Leflunomide-induced CYP1A expression at 72 hpf in wild-type and (D) ahr2^hu3335 mutants. E) Leflunomide-induced CYP1A expression in AHR1B-morphant ahr2^hu3335 larvae and F) ahr2^hu3335 larvae co-injected with AHR1A and AHR1B morpholinos. (G) DMSO control. TCDD-exposed embryos were IHC processed side-by-side and imaged at 120 hpf using the same exposure settings and a single focal plane. Leflunomide-exposed embryos and DMSO control were processed side-by-side and imaged at 72 hpf using the same exposure times; images were created from a z-stack of 10 15.4 uM slices centered on the liver.