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Broadie Laboratory

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

AUTHORS

Bolduc FVFrançois V , Bell K Kimberly , Cox H Hilary , Broadie KS Kendal S , Tully T Tim . Nature neuroscience. 2008 10 ; 11(10). 1143-5

ABSTRACT

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.

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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