J. Dezazzo et al., Developmental expression of an amn(+) transgene rescues the mutant memory defect of amnesiac adults, J NEUROSC, 19(20), 1999, pp. 8740-8746
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.