The neuropeptide FLP-11 induces and self-inhibits sleep through the receptor DMSR-1 in Caenorhabditis elegans. Rossi et al.

Using cell-specific knockdowns, we demonstrate that dmsr-1 induces sleep by acting in cholinergic neurons downstream of RIS activation. Pharmacological intervention indicates that inhibiting cholinergic signaling is necessary for sleep. Consistently, DMSR-1 expression in cholinergic neurons is essential for core sleep functions, including protective gene expression and survival. In contrast, we found that dmsr-1 in RIS mediates a negative feedback control during sleep, which limits RIS calcium activation and the duration of sleep. Consequently, dmsr-1 in RIS inhibits protective gene expression and survival. Thus, DMSR-1 can control both the initiation and limitation of sleep, effectively coupling sleep induction with a sleep-stop signal. RFamide neuropeptide-GPCR signaling might underlie similar dual mechanisms of sleep control in other species, and self-inhibition of sleep-active neurons might represent a conserved mechanism for limiting the duration of sleep.
This dataset is organized in folders, one for each figure in the manuscript considering main figures and supplementary figures. Inside each folder, data is organized in sub-folders. The sub-folder division replicates the one of the panels in the figure legends. Each group of panels correspond to an individual experiment. For each experiment it is provided in form of excel table: raw data extracted as described in the material and methods chapter, the processed data used to draw plots, and data for statistics calculated as explained in materials and methods chapter. Raw data for each experiment are included just in the folder corresponding to the figure where an analysis of that data is shown for the first time. Folders that contains analysis of raw data already included in a previous folder have a text file indicating where to find the corresponding raw data.