[
International Worm Meeting,
2017]
A major challenge in understanding the function and evolution of sleep lies in identifying the mechanisms that offset the vulnerabilities that come with it, such as the inability to forage or escape. The nematode C. elegans has recently been identified as a useful model for the dissection of sleep function and evolution, as animals experience a primitive sleep-like state that is triggered by conditions that cause cellular damage. In response to noxious environmental conditions such as extreme heat, animals enter a state of behavioral quiescence characterized by a reduction in sensory responsiveness and a cessation of feeding and locomotion. This recovery sleep, or RS, appears to be beneficial under certain conditions, as sleepless mutant animals are impaired for survival following noxious heat exposure. We wished to investigate how the decision to enter into RS may be influenced by additional environmental inputs that could potentially alter the physiological benefit to be gained from sleep. Here we show that food deprivation suppresses RS, and that this effect is exacerbated as population density increases. In addition to suppressing sleep drive, food deprivation protects against the lethality associated with sleep loss, suggesting that food-deprived animals have a reduced need for sleep. We show that suppression of sleep drive during periods of food deprivation requires AMP kinase. Additionally, we show that competence to engage in RS is dependent on the neuroendocrine signal DAF-7/TGF- beta , activating a previously identified neural circuit that shifts several aspects of development and metabolism from conservation to utilization of energetic resources. These data suggest that recovery sleep in C. elegans is an energetically costly activity that can be suppressed when environmental conditions are unfavorable and animals are required to compete for resources.