The AKAP Yu is required for olfactory long-term memory formation in Drosophila.

摘要: Extensive neurogenetic analysis has shown that memory formation depends critically on cAMP-protein kinase A (PKA) signaling. Details of how this pathway is involved in formation, however, remain to be fully elucidated. From a large-scale behavioral screen Drosophila, we identified the yu mutant defective one-day after spaced training. The mutation disrupts gene encoding an A-kinase anchoring protein (AKAP). AKAPs comprise family proteins, which determine subcellular localization PKAs and thereby restrict cAMP signaling within cell. Further characterizations revealed long-term (LTM) was disrupted specifically mutant, whereas learning, short-term anesthesia-resistant all appeared normal. Another independently isolated failed complement LTM defect associated with mutation, phenotypic could rescued by induced acute expression yu(+) transgene, suggesting functions physiologically during formation. AKAP Yu expressed preferentially mushroom body (MB) neuroanatomical structure, transgene MB, but not other brain regions, sufficient rescue mutant. These observations lead us conclude proper PKA MB neurons required for LTM.