It's hard to think of a worm curling up in a sunny window and dozing off like a pet cat. But, as David Raizen, MD, PhD, assistant professor of Neurology has shown, they do just that (minus the sunny window part). Studying the classic laboratory research veteran the round worm C. elegans, Raizen and his colleagues identified a definite period of behavioral quiescence that occurs at a certain point in the roundworm's life cycle. Called "lethargus," it's a sleep-like state that coincides with a period of nervous system change and growth. When lethargus is denied or interrupted, growth can be disrupted. Raizen also found that a certain gene in C. elegans, which encodes a protein kinase and is regulated by the cyclic GMP molecule, also seems to play a vital role in the worm's lethargus phase.
In further research on the effects of depriving C. elegans of sleep, Raizen discovered that sleep loss creates stress responses in the roundworm and causes the migration of a protein called DAF-16 from the cell cytoplasm into the nucleus, thereby controlling other stress-related genes. DAF-16 is necessary for a phenomenon called "sleep homeostasis," in which an animal tries to catch up on lost sleep to restore physiological balance. When Raizen and his team knocked out the DAF-16 gene, thus eliminating the sleep homeostatic response, as many as half the roundworms in the study sample died, indicating the importance of the homeostatic behavior. Unexpectedly, homeostasis could be reactivated by restoring DAF-16 to muscle tissue rather than to neurons, which suggests that sleep isn't all just in the brain.