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.
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Bolduc, F., Bell, K., Cox, H. et al. Excess protein synthesis in Drosophila Fragile X mutants impairs long-term memory. Nat Neurosci 11, 1143–1145 (2008). https://doi.org/10.1038/nn.2175
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