Sleep is an emergent behavior that requires concordance of many factors. Most organisms structure their sleep-wake patterns around environmental changes in light and temperature. In parallel to this reactive, sensory-driven component, internal timing mechanisms help control sleep-wake transitions even in the absence of sensory cues. The goal of this project us to identify the circuit and molecular logic of a neural system that controls the timing of sleep in Drosophila melanogaster. My preliminary experiments have identified a novel connection between color photoreceptors and circadian cells. Our early data suggest that this sensory-circadian circuit node may integrate and transmit visual information to sleep- and wake?controlling cells. It's connectivity to downstream sleep and circadian neurons may explain why flies have differential wake- and sleep- promoting responses to light depending on the time of day. Parallel to this discovery, our group identified the photoreceptor gene Retinophilin (RTP) in an unbiased screen for neuronal genes that control sleep. Intriguingly, other genes that act in the same pathway preferentially control the timing of sleep after the lights turn off. These results have led us to investigate the unmapped role of the visual system in regulating wake-sleep transitions. I will use a combination of behavior, circuit mapping, and functional imaging to determine the genes and cells that control the timing of sleep after the lights turn off. I will use the same approaches to determine circuit properties that allow light to promote sleep or wakefulness at different times of day. These experiments will help elucidate why sleep is perturbed when sensory cues are incongruent with circadian signals. The results of these experiments are likely to be relevant to understanding the consequences of light stimulation in more complex animals because features of sleep are highly conserved across species.
In humans, exposure to artificial lighting in the evening affects the timing and quality of sleep. Mechanistic understanding of sleep circuitry is limited, and this is reflected by drugs that do not differentiate between sleep initiation and sleep maintenance deficits. Because the genes controlling circadian rhythms and sleep are conserved across organisms, this project may contribute to the development of tailored interventions into human sleep disorders by building a systematic understanding of where and how circadian and sensory cues interact in the brain.