Description

Across species, sleep is increased following exposure to damaging conditions, a phenomenon known as stress-induced sleep (SIS) (Hill et al. 2014; Lenz et al. 2015; Zada et al. 2019). In C. elegans, SIS is dependent on the ALA interneuron (Hill et al. 2014; Nelson et al. 2014), which promotes a coordinated quiescent state through the collective action of several neuropeptides (Nelson et al. 2014; Nath et al. 2016). Recently it has been shown that ALA ablation can suppress phenotypes associated with loss of the cephalic sensilla sheath (CEPsh) glia, such as prolonged larval development and locomotor pausing in adults (Katz et al. 2018), indicating that these glia attenuate certain aspects of ALA function. The CEPsh glia form a tubular structure surrounding the sensory endings of the CEP neurons and also extend thin processes that sheath the nerve ring, including the synapse between ALA and the postsynaptic AVE, a major locomotor interneuron. While the ALA is likely to promote SIS via peptidergic rather than synaptic signaling (Nelson et al. 2014; Nath et al. 2016), we wished to determine whether CEPsh glia ablation may impact the SIS-promoting function of ALA. To this end, we examined three independent lines that genetically ablate the four CEPsh glial cells (Katz et al. 2018), and compared the SIS responses of these strains to wild type and to ALA specification-defective ceh-17(np1) mutant animals. We examined three conditions known to trigger ALA-dependent sleep: noxious heat, pore-forming Cry5B toxin, and ultraviolet light exposure (Figure 1). We found that while the glia-ablated (GA) lines displayed a trend toward enhanced heat-SIS at the 15min time point, there were no significant differences in heat-SIS between the GA lines and wild-type. The GA lines also showed wild-type Cry5B-SIS. Surprisingly, two of the GA lines showed reduced UV-SIS, rather than the enhanced sleep that would be predicted if the CEPsh glia attenuate ALA’s peptidergic function. Our data indicate that CEPsh glia are largely dispensable for stress-induced sleep, but may modulate the UV–SIS response. As UV exposure elicits a delayed sleep response relative to other SIS triggers, we speculate that UV damage may activate ALA in a manner that is distinct, and partially supported by glial function.