Stress-Induced Sleep After Exposure to Ultraviolet Light Is Promoted by p53 in .

Stress-induced sleep (SIS) in is important for restoration of cellular homeostasis and is a useful model to study the function and regulation of sleep. SIS is triggered when epidermal growth factor (EGF) activates the ALA neuron, which then releases neuropeptides to promote sleep. To further understand this behavior, we established a new model of SIS using irradiation by ultraviolet C (UVC) light. While UVC irradiation requires ALA signaling and leads to a sleep state similar to that induced by heat and other stressors, it does not induce the proteostatic stress seen with heat exposure. Based on the known genotoxic effects of UVC irradiation, we tested two genes, and , which encode proteins that act in the DNA damage response pathway. Loss-of-function mutants of had no defect in UVC-induced SIS but a partial loss-of-function mutant of , , had decreased movement quiescence following UVC irradiation. Germline ablation experiments and tissue-specific RNA interference experiments showed that is required somatically in neurons for its effect on SIS. The () mutant suppressed body movement quiescence controlled by EGF, indicating that CEP-1 acts downstream or in parallel to ALA activation to promote quiescence in response to ultraviolet light.