Excess protein synthesis in Drosophila Fragile X mutants impairs long-term memory

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Abstract
It was previously known that a lack of FMRP can lead to a broad increase in protein synthesis. In this manuscript, the authors demonstrate a direct association between enhanced protein synthesis and the cognitive deficits observed in animal models lacking FMRP. We used Drosophila olfactory memory as a model to study the molecular basis of cognitive defects in Fragile X syndrome in vivo. We observed that fragile X protein was acutely required and interacted with argonaute1 and staufen in the formation of long-term memory. Occlusion of long-term memory formation in Fragile X mutants could be rescued by protein synthesis inhibitors, suggesting that excess baseline protein synthesis could negatively affect cognition.