0010 CHARACTERIZING THE INFLUENCE OF THE MOLECULAR CIRCADIAN CLOCK ON SLEEP ARCHITECTURE IN DROSOPHILA MELANOGASTER

Abstract

The daily timing of sleep is controlled by a circadian clock, the disruption of which is physiologically and psychologically detrimental. While an identified network of circadian clock neurons controls the timing of sleep, a comprehensive understanding of how each of the components of the molecular clock affect sleep architecture is lacking. Though the loss of the circadian clock does not prevent sleep, it results in drastic changes in the quality of sleep. To better understand the ways in which the circadian clock governs sleep, we sought to systematically characterize the impact of loss of function mutations in Clock, cycle, period, and timeless on the sleep rhythm and sleep architecture in Drosophila under both entrained and free-running conditions and to investigate the role light plays in in the regulation of sleep in wild-type and mutant flies. Using the Drosophila activity monitoring system, we measured sleep in flies bearing loss of function mutations in the Clock (Clkjrk), cycle (cyc01), period (per01), and timeless (tim01) genes. Sleep was measured in under a 12:12h Light/Dark cycle, constant darkness, and constant light. To assess the impact of light on sleep, sleep was measured under various wavelengths and intensities. Our analysis of sleep in these lines reveals that all four mutations caused fragmented sleep. Loss of function mutations within the negative limb of the clock (i.e., per01 and tim01) resulted in altered daytime sleep architecture but no changes in total sleep time for over the diurnal or circadian cycle. Loss of function mutations in the positive limb of the circadian clock (i.e., Clkjrk and cyc01) result not only in significantly decreased sleep but also reveal a sleep promoting effect of light. We found that loss of function mutations in circadian clock genes resulted in significant effects on sleep quality with mutations in the negative and positive limb genes producing remarkably different phenotypes. none.