Members of the transforming growth factor beta (TGF-β) family of secreted factors play critical roles in development across species. In the nematode C. elegans, the DAF-7/TGF-β ligand is part of a signaling cascade that determines developmental, metabolic, and behavioral decisions based on environmental conditions. During larval development, favorable environmental conditions activate a conventional TGF-β signaling cascade that promotes reproductive growth by stimulating the production of a hormone, dafachronic acid (DA). In the absence of this signal, the animal delays reproduction and growth by entering into an alternate life stage known as dauer. In addition to its roles during development, TGF-β signaling has known roles during the adult stage, including pathogen avoidance and longevity. Here, we describe a previously unknown physiological role for TGF-β signaling in sleep behavior. C. elegans is known to sleep following exposure to noxious environmental conditions that cause cellular stress, such as heat. This stress-induced sleep (SIS) response is mediated by activation of epidermal growth factor (EGF) signaling in a sleep-inducing neuron called ALA, and induction of EGF-overexpression (EGF-OE) promotes a robust sleep response in the absence of noxious stress. We have identified that daf-7/TGF-β mutants are impaired for SIS, and intriguingly, that various aspects of the sleep program are differentially affected. By exposing daf-7 mutants to a variety of stressors and examining their sleep behavior, we have determined that daf-7 mutants are severely impaired for locomotor quiescence but only mildly impaired for feeding quiescence. We wished to ascertain where in the SIS pathway DAF-7 is acting. To test this, we overexpressed the EGF ligand and examined daf-7 mutants for sleep behavior. Interestingly, we found that daf-7 mutants are still slightly impaired for sleep in response to EGF-OE. This suggests that the primary effects of DAF-7 on SIS may be downstream of EGF. To determine whether the role of DAF-7 in sleep regulation is dependent on DA hormone signaling, we examined daf-36 and daf-12 mutants, which are defective in the production of DA and its receptor, respectively. Both mutants displayed very mild defects in SIS, indicating that the effects of DAF-7 are attributable partially to dafachronic acid production during development and partly to an unidentified mechanism. I am currently analyzing changes in daf-7 expression in response to stress. We speculate that DAF-7 may be conferring competency on the ALA neuron to mediate discrete aspects of EGF-induced sleep. Therefore, I plan to analyze reporter genes corresponding to ALA-expressed components of stress-induced sleep.