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The Journal of Neuroscience, October 15, 1999, 19(20):8740-8746

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

James DeZazzo, Shouzhen Xia, Jeff Christensen, Klara Velinzon, and Tim Tully

Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724

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 amn transcript is involved in adult memory formation. With the use of a UAS-amn+ transgene, we show complete rescue of memory defects in amn28A, a mutant allele caused by the insertion of a GAL4 enhancer trap transposon (Moore et al., 1998). Study of the amn28A 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.

Key words: Drosophila; neuropeptide; Pavlovian learning; neurogenetics; mutants; behavioral rescue; olfactory memory; associative learning; neurodevelopment; cAMP signaling; ethanol sensitivity


Copyright © 1999 Society for Neuroscience  0270-6474/99/19208740-07$05.00/0


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