The Drosophila memory gene amnesiac(amn) has been proposed to encode a neuropeptide protein, which includes regions homologous to vertebrate pituitary adenylyl cyclase-activating peptide (PACAP; ). Definitive experiments to link this gene to memory formation, however, have not yet been accomplished (). The experiments described here demonstrate that the putative amntranscript is involved in adult memory formation. With the use of aUAS–amn+ transgene, we show complete rescue of memory defects in amn28A, a mutant allele caused by the insertion of a GAL4 enhancer trap transposon (). Study of theamn28A reporter reveals widespread expression in the adult brain but also enriched expression in the embryonic and larval nervous systems. To begin addressing the temporal requirement of amn in memory, we asked whether the memory defects could be rescued by restricting transgenic expression to the adult stage. A heat-shock regimen shown previously to rescue fully the amn ethanol sensitivity defect () failed to rescue the memory defect. These results, coupled with previous genetic and anatomical studies, suggest that adult memory formation and ethanol sensitivity have different temporal and spatial requirements for amn.
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