ArticleCurrent biology : CB2011
Notch signaling modulates sleep homeostasis and learning after sleep deprivation in Drosophila.
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 50 papers, 1 of them a synthesis that pooled it.
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50 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
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- The Sleep Nullifying Apparatus: A Highly Efficient Method of Sleep Depriving Drosophila.Journal of visualized experiments : JoVE · 2020Article
- Natural selection on sleep duration in Drosophila melanogaster.Scientific reports · 2020Article
- Spen modulates lipid droplet content in adult Drosophila glial cells and protects against paraquat toxicity.Scientific reports · 2020Article
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- The Glial Perspective on Sleep and Circadian Rhythms.Annual review of neuroscience · 2020Review
- Post-Developmental Roles of Notch Signaling in the Nervous System.Biomolecules · 2020Review
- Pumilio Regulates Sleep Homeostasis in Response to Chronic Sleep Deprivation inFrontiers in neuroscience · 2020Article
- Review
- A Secreted Ig-Domain Protein Required in Both Astrocytes and Neurons for Regulation of Drosophila Night Sleep.Current biology : CB · 2019Article
- Endocytosis at theeLife · 2018Article
- The neurobiological basis of sleep: Insights from Drosophila.Neuroscience and biobehavioral reviews · 2018Review
- The DSL ligand APX-1 is required for normal ovulation in C. elegans.Developmental biology · 2018Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
The role of the transmembrane receptor Notch in the adult brain is poorly understood. Here, we provide evidence that bunched, a negative regulator of Notch, is involved in sleep homeostasis. Genetic evidence indicates that interfering with bunched activity in the mushroom bodies (MBs) abolishes sleep homeostasis. Combining bunched and Delta loss-of-function mutations rescues normal homeostasis, suggesting that Notch signaling may be involved in regulating sensitivity to sleep loss. Preventing the downregulation of Delta by overexpressing a wild-type transgene in MBs reduces sleep homeostasis and, importantly, prevents learning impairments induced by sleep deprivation. Similar resistance to sleep loss is observed with Notch(spl-1) gain-of-function mutants. Immunohistochemistry reveals that the Notch receptor is expressed in glia, whereas Delta is localized in neurons. Importantly, the expression in glia of the intracellular domain of Notch, a dominant activated form of the receptor, is sufficient to prevent learning deficits after sleep deprivation. Together, these results identify a novel neuron-glia signaling pathway dependent on Notch and regulated by bunched. These data highlight the emerging role of neuron-glia interactions in regulating both sleep and learning impairments associated with sleep loss.
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