Abstract
Neurodevelopmental disorders (NDDs) are a heterogenous group of disorders that impact approximately one in six individuals in the United States. Genetics play a key role in the onset of NDDs but emerging evidence indicates that NDDs often result from the combination of genetic and environmental risk factors. Bisphenols are pervasive environmental chemicals used to produce polycarbonate plastics and epoxy resins. The most well-known bisphenol—bisphenol A (BPA)—is a well-established endocrine disrupting chemical, but more recent studies have also linked BPA exposure to abnormal neurodevelopment and nervous system function in several model organisms. Due to its established harmful effects BPA has been removed from some commercial products; however, manufacturers often replace BPA with chemical analogues, like bisphenol F (BPF). BPF has undergone far less toxicology testing than BPA, and due to its structural similarity with BPA, BPF may have similar harmful effects. Our aim is to use Drosophila melanogaster to determine if BPF disrupts neurodevelopment on its own or in combination with the Drosophila ortholog of FMR1 (fmr1) by examining embryonic survival, naïve courtship behaviors, and axon outgrowth in mushroom body of adult flies. Here we show preliminary data that suggests that exposure to BPF reduces embryonic survival to adulthood and reduces courtship indices in a wild-type genetic background.