In epidemiological studies, prenatal cortisol exposure has been linked to increased autism spectrum disorder (ASD) prevalence. Cortisol is the primary hormone released in the body in response to stress and plays a key role in development. Fragile X syndrome (FXS) is the most common inherited form of intellectual disability, and 30–50% of children with FXS are also diagnosed with ASD. FXS is caused by loss of function mutations in the FMR1 gene on the X chromosome. Our objective was to investigate how embryonic cortisol exposure interacts with FMR1 loss by assessing transcriptome changes in cortisol-treated fmr1 knockout zebrafish embryos. Embryos from wild-type zebrafish and fmr1 knockout zebrafish were exposed to 5uM cortisol solution or vehicle solution at 6 hours post fertilization. Total RNA samples were isolated at 24-, 48-, 72-, and 120-hours post-fertilization (hpf). Sample quality was assessed by spectrophotometry, and RNA concentrations were determined by DNA-binding fluorescent dye methods. Samples will be submitted for RNA-seq analysis to test for genotype-dependent, treatment-dependent, and gene x treatment interactions in terms of neurodevelopmental gene expression across timepoints. These results will help characterize the interaction of embryonic cortisol exposure and FXS genotype in terms of gene expression regulation.
