NPR-1 modulates plasticity in C. elegans stress-induced sleep, Soto et al., 2019

This data set corresponds to the six main-text figures and the one supplemental figure of Soto et al., 2019, a study on the role of the neuropeptide receptor NPR-1 in C. elegans stress-induced sleep (SIS). Sleep is beneficial yet antagonistic to critical functions such as foraging and escape, and we aim to understand how these competing drives are functionally integrated. C. elegans, which lives in reduced oxygen environments, engages in developmentally timed sleep (DTS) during larval stage transitions and engages in stress-induced sleep (SIS) during recovery from damaging conditions. While DTS and SIS use distinct mechanisms to coordinate multiple sleep-associated behaviors, we show that movement quiescence in these sleep states is similarly integrated with the competing drive to avoid oxygen. Further, by manipulating oxygen to deprive animals of SIS, we observe sleep rebound in a wild C. elegans isolate, indicating that sleep debt accrues during oxygen-induced SIS deprivation. Our work suggests that multiple sleep states adopt a common, highly plastic effector of movement quiescence that is suppressed by aversive stimuli and responsive to homeostatic sleep pressure, providing a limited window of opportunity for escape.本数据集对应Soto等人2019年研究的6幅正文图及1幅补充图，该研究聚焦于神经肽受体NPR-1在秀丽隐杆线虫（C. elegans）应激诱导睡眠（SIS）中的作用。睡眠虽具有益处，但与觅食、逃逸等关键生理功能存在拮抗作用，本研究旨在阐明这些相互竞争的行为驱动力如何在功能层面实现整合。栖息于低氧环境的秀丽隐杆线虫，在幼虫阶段转变期间会发生发育时序性睡眠（DTS），而在受损状态恢复阶段则会进入应激诱导睡眠（SIS）。尽管发育时序性睡眠与应激诱导睡眠通过不同机制调控多种睡眠相关行为，但本研究发现，这两种睡眠状态下的运动静息状态，均与规避氧气的竞争驱动力实现了相似的功能整合。此外，通过调控氧气浓度以剥夺线虫的应激诱导睡眠，我们在野生型秀丽隐杆线虫分离株中观察到了睡眠反弹现象，这表明在氧气诱导的应激诱导睡眠剥夺期间，睡眠债会不断累积。本研究结果表明，多种睡眠状态共享一套高度可塑性的运动静息调控效应通路：该通路可被厌恶性刺激抑制，并能响应稳态睡眠压力，从而为逃逸行为留下有限的时间窗口。