ArticleCurrent biology : CB2011
C. elegans Notch signaling regulates adult chemosensory response and larval molting quiescence.
Article in Current biology : CB, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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86 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
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- Notch activity is modulated by the aGPCR Latrophilin binding the DSL ligand in C. elegans.Nature communications · 2025Article
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- Essential and dual effects of Notch activity on a natural transdifferentiation event.Nature communications · 2025Article
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- Quiescence Enhances Survival during Viral Infection inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- DOS-3 mediates cell-non-autonomous DAF-16/FOXO activity in antagonizing age-related loss of C. elegans germline stem/progenitor cells.Nature communications · 2024Article
- Evolution and Function of the Notch Signaling Pathway: An Invertebrate Perspective.International journal of molecular sciences · 2024Review
- Aging disrupts spatiotemporal regulation of germline stem cells and niche integrity.Biology open · 2024Article
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26 more citing papers are in PubMed but not listed here.
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13 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundThe conserved DOS-motif proteins OSM-7 and OSM-11 function as coligands with canonical DSL (Delta, Serrate, and LAG-2) ligands to activate C. elegans Notch receptors during development. We report here that Notch ligands, coligands, and the receptors LIN-12 and GLP-1 regulate two C. elegans behaviors: chemosensory avoidance of octanol and quiescence during molting lethargus.
resultsC. elegans lacking osm-7 or osm-11 are defective in their response to octanol. We find that OSM-11 is secreted from hypodermal seam cells into the pseudocoelomic body cavity and acts non-cell autonomously as a diffusible factor. OSM-11 acts with the DSL ligand LAG-2 to activate LIN-12 and GLP-1 Notch receptors in the neurons of adult animals, thereby regulating octanol avoidance response. In adult animals, overexpression of osm-11 and consequent Notch receptor activation induces anachronistic sleep-like quiescence. Perturbation of Notch signaling alters basal activity in adults as well as arousal thresholds and quiescence during molting lethargus. Genetic epistasis studies reveal that Notch signaling regulates quiescence via previously identified circuits and genetic pathways including the egl-4 cGMP-dependent kinase.
conclusionsOur findings indicate that the conserved Notch pathway modulates behavior in adult C. elegans in response to environmental stress. Additionally, Notch signaling regulates sleep-like quiescence in C. elegans, suggesting that Notch may regulate sleep in other species.
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