Intellectual disability is the most common developmental disorder, with an estimated worldwide prevalence of 1%. Although in many cases the causes of intellectual disability are complex, a number of types of intellectual disability are caused by mutations in a single gene. Loss of the ZC3H14 gene, which encodes an evolutionarily conserved polyadenosine RNA binding protein, leads to a form of inherited autosomal recessive intellectual disability. Loss of the fly ZC3H14 ortholog, dNab2, within Drosophila neurons impairs behavior, short-term memory, and alters patterns of axon guidance in the brain. Intriguingly, these brains exhibit longer poly (A) tails and increased levels of m6A (methylation of position-6 in the RNA base adenosine) expression as compared to control flies. The m6A mark is an abundant and reversible RNA modification linked to post-transcriptional gene regulation of mRNA with poorly understood biological relevance. Biochemical data suggest that ZC3H14/dNab2 may interact physically with a metabolic enzyme known to deaminate adenosine monophosphate (AMP), leading to the hypothesis that this enzyme could act on m6A in RNA as well. Our preliminary data reveal strong genetic interactions between dNab2 and the AMP deaminase in a retinal model (GMR-dNab2). These preliminary studies will be followed-up with biochemical and genetic experiments to test the hypothesis that dNab2 controls m6A levels and expression of specific neuronal target RNAs by interacting with an AMP deaminase. These experiments could provide novel insight into how loss of ZC3H14 impairs brain function.