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Rdl Expression Impacts Circadian Rhythm and Locomotion in Drosophila melanogaster

The genes that modulate circadian rhythm in Drosophila melanogaster have been at the forefront of sleep research in an effort to characterize the impact of circadian rhythm on other biological processes and identify potential overlap in human sleep disorders. In flies, Resistant to Dieldrin (Rdl) encodes a subunit of the GABA receptor, which is upregulated by the circadian oscillator, WAKE. This interaction promotes RDL localization to the plasma membrane to modulate sleep; however, the specific function of RDL and its downstream interactions to facilitate sleep/wake switching have yet to be characterized. Prior research has shown that Rdl can suppress kazachoc (kcc), which in turn suppresses paralytic (para). para is known to control voltage‐gated sodium channels (VGSC's) in the same way that the human gene SCN1A does. This is noteworthy because mutations in SCN1A are linked to epilepsy in humans, and mutations in para result in seizure‐like behavior in Drosophila. The Drosophila Activity Monitor TriKinetics System and a custom‐built light controlling apparatus was employed to characterize locomotion in control and RdlMD‐RR mutant flies. Since circadian rhythm is largely influenced by light and dark patterns, the flies were monitored during 12‐hour light and dark cycles over a period of 5 days to determine any variation between genotypes. Analysis of the data show control flies exhibit consistent sleep and wake patterns with peaks of activity in daylight hours, and activity in darkness is significantly reduced. Conversely, RdlMD‐RR flies show less activity during daylight hours, and near paralysis in darkness. These data suggest that Rdl expression is related to restricting locomotion during sleep and that levels may be modulated by circadian oscillation. Future research will focus on characterizing the effect of Rdl on para expression using RT‐qPCR to elucidate the role of RDL in circadian regulation.