Pharmacological inhibition of the RA pathway partially rescues the gdf6a mutant CMZ phenotype. (A-F) Lateral views of eyes from 60hpf gdf6au768 mutants treated with vehicle (DMSO;A,C,E) or the RAR inverse agonist BMS493 (15µM; B,D,F) showing expression of col15a1b (A,B), ccnd1 (C,D) and atoh7 (E,F). The number of embryos with staining pattern similar to that shown is indicated as a fraction in lower right corner of images. (G) qPCR quantification of relative gene expression levels for col15a1b, ccnd1, atoh7 and nr2f5 in 60hpf mutant eyes and eyes from mutants treated with BMS493, normalised to β-actin. Values for each gene from DMSO-treated mutant eyes were set to 1 and fold changes in BMS493-treated eyes were plotted relative to this value (±s.e.).
|