Food-dependent plasticity in caenorhabditis elegans stress-induced sleep is mediated by TOR–FOXA and TGF-β signaling

Abstract

Behavioral plasticity allows for context-dependent prioritization of competing drives, such as sleep and foraging. Despite the identification of neuropeptides and hormones implicated in dual control of sleep drive and appetite, our understanding of the mechanism underlying the conserved sleep-suppressing effect of food deprivation is limited. Caenorhabditis elegans provides an intriguing model for the dissection of sleep function and regulation as these nematodes engage a quiescence program following exposure to noxious conditions, a phenomenon known as stress-induced sleep (SIS). Here we show that food deprivation potently suppresses SIS, an effect enhanced at high population density. We present evidence that food deprivation reduces the need to sleep, protecting against the lethality associated with defective SIS. Additionally, we find that SIS is regulated by both target of rapamycin and transforming growth factor-β nutrient signaling pathways, thus identifying mechanisms coordinating sleep drive with internal and external indicators of food availability.