Developmental Expression of an amn⁺ Transgene Rescues the Mutant Memory Defect of amnesiacAdults

Abstract

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; Feany and Quinn, 1995). Definitive experiments to link this gene to memory formation, however, have not yet been accomplished (Kandel and Abel, 1995). 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 amn^28A, a mutant allele caused by the insertion of a GAL4 enhancer trap transposon (Moore et al., 1998). Study of theamn^28A 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 (Moore et al., 1998) 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.