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

• Published in: Nature neuroscience Vol. 11; no. 10; pp. 1143 - 1145
• Main Authors: Bell, Kimberly, Tully, Tim, Bolduc, François V, Broadie, Kendal S, Cox, Hilary
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01.10.2008; Nature Publishing Group
• Subjects: Analysis of Variance; Animal Genetics and Genomics; Animals; Animals, Genetically Modified; Behavior, Animal; Behavioral Sciences; Biological Techniques; Biomedical and Life Sciences; Biomedicine; brief-communication; Conditioning, Classical - physiology; Disease Models, Animal; Drosophila; Drosophila Proteins - genetics; Electroshock; Fragile X Mental Retardation Protein - genetics; Fragile X Syndrome - complications; Fragile X Syndrome - metabolism; Genotype & phenotype; Insects; Intellectual disabilities; Memory; Memory Disorders - etiology; Mental retardation; Mutation; Neurobiology; Neurosciences; Olfactory Pathways - physiology; Protein biosynthesis; Protein Biosynthesis - drug effects; Protein Biosynthesis - physiology; Protein synthesis; Proteins; Risk factors; RNA Interference; Space Perception - physiology; Time Factors; United States; United States > US
• ISSN: 1097-6256; 1546-1726
• DOI: 10.1038/nn.2175

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.