Amazed how you are unable to wake-up before loading up on seven to eight hours of sleep while your co-worker seems to function fine with just four hours in bed? According to a study, you can blame the difference on genetic variability.
The researchers report that two genes are required for normal slumber in fly models of sleep: taranis and cyclin-dependent kinase 1 (Cdk1). "Our research elucidates a new molecular pathway and a novel brain area that plays a role in controlling how long we sleep," said senior study author Kyunghee Koh, assistant professor of Neuroscience at the US's Thomas Jefferson University.
"There is a lot we do not understand about sleep, especially when it comes to the protein machinery that initiates the process on the cellular level." The researchers examined thousands of mutant fly lines and found a mutant, called taranis, which slept a lot less than normal flies. The researchers tracked how taranis interacted with other proteins and saw that taranis is bound to a known sleep regulator protein called cyclin A. Their data suggests that taranis and cyclin A create a molecular machine that inactivates Cdk1, whose normal function is to suppress sleep and promote wakefulness.
Previous research has shown that cyclin A is expressed in a small number of neurons including a cluster of seven neurons on each side of the brain. Koh and colleagues showed that these neurons are located in an area of the fly brain that corresponds with the human hypothalamus - one of the sleep centres of the human brain. They saw a reduction of overall sleep when taranis was knocked down only in these 14 neurons and when these same neurons are activated. "We think this may be an arousal centre in the fly brain that taranis helps inhibit during sleep."
Although the taranis protein has a human cousin, called the Trip-Br family of transcriptional regulators, it is yet unclear whether a similar system is at play in humans.
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