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.
MeSH terms
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Analysis of Variance
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Animals
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Animals, Genetically Modified
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Behavior, Animal
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Conditioning, Classical / physiology
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Disease Models, Animal*
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Drosophila
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Drosophila Proteins / genetics
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Electroshock
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Fragile X Mental Retardation Protein / genetics
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Fragile X Syndrome / complications*
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Fragile X Syndrome / metabolism*
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Memory Disorders / etiology*
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Mutation
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Olfactory Pathways / physiology
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Protein Biosynthesis / drug effects
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Protein Biosynthesis / physiology*
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RNA Interference
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Space Perception / physiology
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Time Factors
Substances
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Drosophila Proteins
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Fragile X Mental Retardation Protein