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Abstract
Glutamate receptors (GluR) assist with learning and memory. Disruptions in the molecular pathways required for production or localization of GluRs are implicated in neurological disorders such as Alzheimer's disease. This study was undertaken to evaluate the role of Lk6, a translational regulatory protein, in GluR translation, using the model organism Drosophila melanogaster. Preliminary data has shown that lk6 mutants exhibit a significant reduction in the level of GluRs localizing to the synapse but a significant increase in the level of GluR mRNA being produced. Decreasing the expression of eIF4E showed lower levels of GluR localization. Mutations in lk6 or eIF4E in conjunction with inhibitors of target of rapamycin, a translational pathway inhibitor, also showed significant reduction in the level of synaptic GluRs. The results of this study support the hypothesis that Lk6 is necessary for normal expression of GluRs.
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