Regulation of Satiety Quiescence by Neuropeptide Signaling in Caenorhabditis elegans
| Autor: | Young-Jai You, Jeongho Kim, Enkhjin Ulzii, Mei Makino, Riku Shirasaki |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Interneuron satiety Neuropeptide Neurosciences. Biological psychiatry. Neuropsychiatry neural circuit medicine.disease_cause TGFβ 03 medical and health sciences 0302 clinical medicine cyclic GMP RNA interference Sleep and metabolism TGF beta signaling pathway medicine quiescence Caenorhabditis elegans Mutation biology General Neuroscience biology.organism_classification Sleep in non-human animals Cell biology 030104 developmental biology medicine.anatomical_structure metabolism 030217 neurology & neurosurgery RC321-571 |
| Zdroj: | Frontiers in Neuroscience, Vol 15 (2021) |
| ISSN: | 1662-453X |
| DOI: | 10.3389/fnins.2021.678590 |
| Popis: | Sleep and metabolism are interconnected homeostatic states; the sleep cycle can be entrained by the feeding cycle, and perturbation of the sleep often results in dysregulation in metabolism. However, the neuro-molecular mechanism by which metabolism regulates sleep is not fully understood. We investigated how metabolism and feeding regulate sleep using satiety quiescence behavior as a readout in Caenorhabditis elegans, which shares certain key aspects of postprandial sleep in mammals. From an RNA interference-based screen of two neuropeptide families, RFamide-related peptides (FLPs) and insulin-like peptides (INSs), we identified flp-11, known to regulate other types of sleep-like behaviors in C. elegans, as a gene that plays the most significant role in satiety quiescence. A mutation in flp-11 significantly reduces quiescence, whereas over-expression of the gene enhances it. A genetic analysis shows that FLP-11 acts upstream of the cGMP signaling but downstream of the TGFβ pathway, suggesting that TGFβ released from a pair of head sensory neurons (ASI) activates FLP-11 in an interneuron (RIS). Then, cGMP signaling acting in downstream of RIS neurons induces satiety quiescence. Among the 28 INSs genes screened, ins-1, known to play a significant role in starvation-associated behavior working in AIA is inhibitory to satiety quiescence. Our study suggests that specific combinations of neuropeptides are released, and their signals are integrated in order for an animal to gauge its metabolic state and to control satiety quiescence, a feeding-induced sleep-like state in C. elegans. |
| Databáze: | OpenAIRE |
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