Developmental expression of an amn(+) transgene rescues the mutant memory defect of amnesiac adults

The Drosophila memory gene amnesiac (amn) has been proposed to encode a neu ropeptide protein, which includes regions homologous to vertebrate pituitar y adenylyl cyclase-activating peptide (PACAP; Feany and Quinn, 1995). Defin itive experiments to link this gene to memory formation, however, have not yet been accomplished (Kandel and Abel, 1995). The experiments described he re demonstrate that the putative amn transcript is involved in adult memory formation. With the use of a UAS-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 the amn(28A) reporter reveals widespread expression in the adult brain but also enriche d expression in the embryonic and larval nervous systems. To begin addressi ng the temporal requirement of amn in memory, we asked whether the memory d efects could be rescued by restricting transgenic expression to the adult s tage. 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, sugg est that adult memory formation and ethanol sensitivity have different temp oral and spatial requirements for amn.