Fig. 4

Fig. 4

Zebrafish fdx1b^UOB205 homozygous mutants are glucocorticoid deficient.

A, fdx1b^UOB205 homozygous mutants have impaired visual-mediated adaption. When exposed to a lighter environment, fdx1b^UOB205 homozygous mutants are darker in appearance when compared with control siblings, which had a least 1 wild-type allele (fdx1b^+/+ or fdx1b^UOB205/+). B, Cortisol concentrations were determined from fdx1b^UOB205 homozygous mutant larvae (fdx1b^UOB205) and sibling controls (sib) under basal and stressed conditions. Cortisol was not detected (nd) from fdx1b^UOB205 homozygous mutants under basal conditions. Concentrations were determined from 3 independent replicates and are expressed as picograms per larva (mean ± SD). C, Treatment of fdx1b^UOB205 homozygous mutants with the glucocorticoid agonist dexamethasone (DEX) restored the light adaptation phenotype in contrast to ethanol-treated controls (EtOH). mRNA expression of glucocorticoid response genes (D) pck1 and (E) fkbp5 in fdx1b^UOB205 homozygous mutants and control siblings under basal and stressed conditions. Graphs represent mean relative expression ± SEM (normalized to gapdh). F, Quantitative real-time expression of pomca in fdx1b^{UOB205/UOB205} mutants relative to control siblings. Statistical analysis was performed using one-way ANOVA; *, P < .05; **, P < .01; ***, P < .001.