The most common cause of inherited mental deficiency and monogenetic cause of autism, Fragile X Syndrome (FXS), is one disease that there is little known about its origins and is the focus of this paper. This series of experiments examined the potential role of mRNA deadenylation proteins as contributing factors to the pathogenesis of FXS using Drosophila melanogaster as a model organism. One of the main complexes involved in deadenylation is the CNOT complex, which is comprised of many proteins, including POP2, TWIN, and NOT3. Each protein plays a unique role within the CNOT complex and this study hoped to further characterize these genes. Previous research in the Barbee lab has shown that these genes influence synapse development of the pre-synaptic terminal at the larval neuromuscular junction in D. melanogaster. However, it had not been tested whether POP2, TWIN, and NOT3 also have a post-synaptic effect. The localization of these genes at the neuromuscular junction was also examined and they were found to be concentrated in the pre-synaptic terminal. Finally, this study looked at whether these genes had any role in the development of sensory neurons. There was a significant increase in sensory neuron dendritic growth and a significant decrease in the complexity of the dendritic branches. These results provide insight into the characterization of TWIN, POP2, and NOT3, and their roles within the development of D. melanogaster. Future experiments will examine the genetic and biochemical relationship between the deadenylase complex and FXS in the D. melanogaster model.