Abstract
Considerable evidence indicates that sleep is essential for learning and memory. Drosophila melanogaster has emerged as a novel model for studying sleep. We previously found a short sleeper mutant, fumin (fmn), and identified its mutation in the dopamine transporter gene. We reported similarities in the molecular basis of sleep and arousal regulation between mammals and Drosophila. In aversive olfactory learning tasks, fmn mutants demonstrate defective memory retention, which suggests an association between sleep and memory. In an attempt to discover additional sleep related genes in Drosophila, we carried out a microarray analysis comparing mRNA expression in heads of fmn and control flies and found that 563 genes are differentially expressed. Next, using the pan-neuronal Gal4 driver elav-Gal4 and UAS-RNA interference (RNAi) to knockdown individual genes, we performed a functional screen. We found that knockdown of the NMDA type glutamate receptor channel gene (Nmdar1) (also known as dNR1) reduced sleep. The NMDA receptor (NMDAR) plays an important role in learning and memory both in Drosophila and mammals. The application of the NMDAR antagonist, MK-801, reduced sleep in control flies, but not in fmn. These results suggest that NMDAR promotes sleep regulation in Drosophila.
Highlights
Sleep is a physiological state with unique characteristics
This study provides evidence that NMDA receptor (NMDAR) is involved in the regulation of sleep in flies
To identify molecular candidates involved in sleep and arousal, we performed a genomewide screen of genes that were differentially expressed in heads of control and fmn flies
Summary
Sleep is a physiological state with unique characteristics. Behaviorally, sleep constitutes a consolidated period of rest and immobility without bulky movements, accompanied by an apparent reduced responsiveness to outside stimuli. Sleep-like resting states were described first in the cockroach [3] and in the fruit fly, Drosophila melanogaster [4, 5]. We discovered a mutant with a reduced amount of these sleep-like states, and named it fumin, meaning 'insomnia' in Japanese and identified the mutation in the dopamine transporter gene [6]. This was a striking finding, since dopamine is used to maintain wakefulness in the mammalian brain.
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