Food-dependent plasticity in C. elegans stress-induced sleep is mediated by TOR-FOXA and TGF-beta signaling

Plasticity in the drive to sleep represents an important strategy of coordinating and prioritizing competing behavioral drives to offset some of the vulnerabilities associated with sleep, such as the inability to forage. Despite the identification of various neuropeptides and hormones implicated in the dual control of sleep drive and appetite, the mechanism underlying the sleep-suppressing effect of starvation is poorly understood. 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. This stress-induced sleep (SIS) appears to be beneficial under certain conditions, as sleepless mutant animals are impaired for survival following noxious heat exposure. 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 TOR and TGF-β nutrient signaling pathways, thus identifying mechanisms coordinating sleep drive with internal and external indicators of food availability.

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