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


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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Figure 1: Drosophila FMRP is required for olfactory learning and 1-d memory after spaced training.
Figure 2: Drosophila FMRP is required acutely for LTM formation and interacts with Staufen and Argonaute 1.
Figure 3: Inhibition of protein synthesis ameliorates the LTM defects of Fmr1 mutants.


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F.V.B. conceptualized the project, conducted experiments and wrote the manuscript. K.B. carried out behavioral experiments, H.C. performed the imaging experiments and K.S.B. helped with conceptualization. T.T. conceptualized, supervised and funded the project and wrote the manuscript.

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Correspondence to Tim Tully.

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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).

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