“Ten more minutes, that’s all I need!”—so goes the familiar cry of many early morning risers pleading with their brains to give them a few extra minutes of restful slumber. The antithesis being those, who we secretly hate, that pop out of bed refreshed, ready to start the day, and on seemingly less than the seven to eight hours of sleep that the rest of the population needs to function. Do these perky morning risers have a better mattress than the rest of us? Are they better at counting sheep? Do they possess magical sleeping potions? Instead, perhaps the difference among these populations is largely due to genetic variability.
Researchers from the Farber Institute for Neuroscience at Thomas Jefferson University are siding with the genetic variability theory. They recently reported on the discovery of two genes, originally known for their roles in cell division, that are required for normal sleep patterns in Drosophila melanogaster.
“There's a lot we don't understand about sleep, especially when it comes to the protein machinery that initiates the process on the cellular level,” explained Kyunghee Koh, Ph.D., assistant professor of neuroscience at the Farber Institute for Neurosciences at Thomas Jefferson University and senior author on the study. “Our research elucidates a new molecular pathway and a novel brain area that play a role in controlling how long we sleep.”
Using a forward genetic screen, the researchers examined thousands of mutant fly lines and isolated a gene, Taranis, which they classified as a novel sleep gene associated with a marked reduction in total sleep time. Moreover, when the Jefferson team tracked how Taranis interacted with other proteins, they observed that it bound to a known sleep regulator, Cyclin A—suggesting that Taranis and Cyclin A create a molecular machine that inactivates Cdk1, an enzyme whose normal function is to suppress sleep and promote wakefulness.
The findings from this study were published June 18 in Current Biology through an article entitled “TARANIS Functions with Cyclin A and Cdk1 in a Novel Arousal Center to Control Sleep in Drosophila.”
Previous research into the molecular mechanisms of sleep has shown that Cyclin A is expressed in a small number of neurons located in an area of the fly brain that is analogous to the human hypothalamus, a well-known sleep center of the human brain. Additionally, Dr. Koh’s team able to knockdown Taranis within Drosophila and localize sleep activity to discreet clusters of neurons on both sides of the fly’s brain.
“We think this may be an arousal center in the fly brain that Taranis helps inhibit during sleep,” stayed Dr.Koh.
Dr. Koh and her team were excited about their findings, but understand that they have a long road ahead of them to determine if this mechanism is relevant within the human brain. Interestingly though, the Taranis protein does have a human homolog called the Trip-Br family of transcriptional activators, yet it is unclear as to the role, if any, this protein has in human sleep cycle.