Abstract
SummaryThe daily light-dark cycles represent a key signal for synchronizing circadian clocks. Both insects and mammals possess dedicated “circadian” photoreceptors but also utilize the visual system for clock resetting. In Drosophila, circadian clock resetting is achieved by the blue-light photoreceptor cryptochrome (CRY), which is expressed within subsets of the brain clock neurons. In addition, rhodopsin-expressing photoreceptor cells contribute to light synchronization. Light resets the molecular clock by CRY-dependent degradation of the clock protein Timeless (TIM), although in specific subsets of key circadian pacemaker neurons, including the small ventral lateral neurons (s-LNvs), TIM and Period (PER) oscillations can be synchronized by light independent of CRY and canonical visual Rhodopsin phototransduction. Here, we show that at least three of the seven Drosophila rhodopsins can utilize an alternative transduction mechanism involving the same α-subunit of the heterotrimeric G protein operating in canonical visual phototransduction (Gq). Surprisingly, in mutants lacking the canonical phospholipase C-β (PLC-β) encoded by the no receptor potential A (norpA) gene, we uncovered a novel transduction pathway using a different PLC-β encoded by the Plc21C gene. This novel pathway is important for behavioral clock resetting to semi-natural light-dark cycles and mediates light-dependent molecular synchronization within the s-LNv clock neurons. The same pathway appears to be responsible for norpA-independent light responses in the compound eye. We show that Rhodopsin 5 (Rh5) and Rh6, present in the R8 subset of retinal photoreceptor cells, drive both the long-term circadian and rapid light responses in the eye.
Highlights
Circadian clocks regulate the physiology, behavior, and sleep of organisms in a rhythmic daily fashion
NorpA-Independent Circadian Clock Resetting Requires Gq As a measure of circadian clock synchronization to light, wildtype and mutant flies were raised in 12-hr:12-hr LD cycles at a constant temperature of 25C and 60% relative humidity
We tested flies lacking Rhodopsin 1 (Rh1) in the same norpAP41 cryb background and found that they, too, are not able to resynchronize to LD cycles, suggesting that Rh1 can signal independently of no receptor potential A (norpA) (Figure 2C)
Summary
Circadian clocks regulate the physiology, behavior, and sleep of organisms in a rhythmic daily fashion Proper timing of these parameters contributes to overall fitness, and it is, crucial that circadian clocks are accurately synchronized with the environmental time, dictated by the natural daily cycles of light and temperature [1]. PER and TIM translocate to the nucleus and block CLK/CYC activity to shut down their own transcription until eventual degradation of PER and TIM restarts the cycle [2]. These molecular oscillations can be synchronized to the environment by light-induced degradation of TIM, which is mediated by the blue light photoreceptor cryptochrome (CRY) [3, 4]. Because PER stability depends on the presence and binding to TIM, this pathway efficiently resets the circadian clock to light
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