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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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