Fragile X Syndrome (FXS) is a genetic condition caused by mutations in the fragile X messenger ribonucleoprotein 1 gene (FMR1) on the X chromosome. FXS is the most common inherited form of intellectual disability causing symptoms such as autism spectrum disorder (ASD). Studies have suggested links between higher prenatal cortisol levels and increased frequency of ASD. The purpose of this study was to compare how embryonic cortisol exposure influences early development in wildtype zebrafish embryos and fmr1 knockout zebrafish embryos at 48 hours post fertilization and 72 hours post fertilization (hpf). Zebrafish embryos were collected and dispersed into petri dishes and treated at 6hpf with cortisol concentrations of 0uM, 10uM, 25uM, or 250uM. At 48 hpf and 72 hpf, embryos were dechorionated and imaged via brightfield microscopy to assess developmental phenotypes. Embryos were analyzed and scored for severity of phenotypes, including pericardial edema, spine curvature, eye size, yolk sac abnormalities, and body size. Survival and phenotype severity were then compared between the genotypes across 48 hpf and 72 hpf. This analysis defines morphological sensitivity to cortisol exposure at different developmental stages. Comparison of wildtype zebrafish embryos to fmr1 knockout zebrafish embryos also provides insight into FXS gene-environment interactions.
