“Sleep is vitally important in helping both people and animals to recover during sickness,” said senior author David M. Raizen, MD, PhD, an associate professor of Neurology and a member of the Center for Sleep and Circadian Neurobiology. “Similar signaling may operate in humans and other animals to regulate sleep during sickness. These findings create a launching pad towards future research into the mechanisms for illness-induced sleepiness in humans and other organisms.”
These findings reveal that FLP-13 causes sleep by turning down activity in the nervous system cells that help keep an organism awake. Researchers examined genetic mutations to determine which genes cause the worms to fall asleep when FLP-13 is released. This revealed that worms with mutations that cause them to lack a receptor protein called DMSR-1 on cell surfaces do not become sleepy in response to FLP-13. This indicates that DMSR-1 is essential for FLP-13 to trigger sleep.
Funding was provided by the National Institutes of Health R01NS088432, R21NS091500, and P30ES013508, the European Research Council ERC-2013-ADG-340318, and the Fonds Wetenschappelijk Onderzoek.