ArticleProceedings of the National Academy of Sciences of the United States of America2017
Notch1 maintains dormancy of olfactory horizontal basal cells, a reserve neural stem cell.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 85 citations in OpenAlex.
- Aging-related olfactory loss is associated with olfactory stem cell transcriptional alterations in humans.The Journal of clinical investigation · 2022Trial
- Olfactory mucosal inflammation and barrier disruption correlate with perceived CRSwNP-associated olfactory dysfunction.The World Allergy Organization journal · 2026Article
- Olfactory epithelium regeneration and homeostasis: cellular and molecular mechanisms and novel methodological advances.Cell regeneration (London, England) · 2026Review
- A spatial code governs olfactory receptor choice and aligns sensory maps in the nose and brain.Cell · 2026Article
- FAK inhibition following acute olfactory epithelial inflammation promotes neurogenesis and functional recovery through stem cell CNTF.Stem cells (Dayton, Ohio) · 2026Article
- Deciphering the microenvironment of adult neurogenesis: a perspective from neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Asymmetric histone inheritance regulates olfactory stem cell fates during regeneration.Nature communications · 2026Article
- Lgr5 positive stem cells sustain homeostasis and drive regeneration of the nasal septum olfactory epithelium.Cell and tissue research · 2026Article
- Epitranscriptomics as a Candidate Universal Modulator of Dormancy Transitions.Ecology and evolution · 2026Review
- Mechanical constraints on cell plasticity: insights from the olfactory epithelium.Frontiers in cell and developmental biology · 2026Review
- Progenitor neighborhoods function as transient niches to sustain olfactory neurogenesis.Stem cell reports · 2025Article
- Stem Cell Niches for Olfactory Regeneration and Their Therapeutic Applications.Journal of rhinology : official journal of the Korean Rhinologic Society · 2025Review
- Quiescent horizontal basal stem cells act as a niche for olfactory neurogenesis in a mouse 3D organoid model.Cell reports methods · 2025Article
- Aging and chronic inflammation: impacts on olfactory dysfunction-a comprehensive review.Cellular and molecular life sciences : CMLS · 2025Review
- Mechanisms of Neuronal Differentiation and Notch Signaling as a Potential Therapeutic Target in Olfactory Dysfunction of Allergic Rhinitis.Journal of inflammation research · 2025Article
- Neuroimmune interactions in the olfactory epithelium: maintaining a sensory organ at an immune barrier interface.Trends in immunology · 2024Review
- An in vitro model of acute horizontal basal cell activation reveals gene regulatory networks underlying the nascent activation phase.Stem cell reports · 2024Article
- Article
- Olfactory dysfunction and the role of stem cells in the regeneration of olfactory neurons.Heliyon · 2024Review
- Type 2 and Non-type 2 Inflammation in the Upper Airways: Cellular and Molecular Alterations in Olfactory Neuroepithelium Cell Populations.Current allergy and asthma reports · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The remarkable capacity of the adult olfactory epithelium (OE) to regenerate fully both neurosensory and nonneuronal cell types after severe epithelial injury depends on life-long persistence of two stem cell populations: the horizontal basal cells (HBCs), which are quiescent and held in reserve, and mitotically active globose basal cells. It has recently been demonstrated that down-regulation of the ΔN form of the transcription factor p63 is both necessary and sufficient to release HBCs from dormancy. However, the mechanisms by which p63 is down-regulated after acute OE injury remain unknown. To identify the cellular source of potential signaling mechanisms, we assessed HBC activation after neuron-only and sustentacular cell death. We found that ablation of sustentacular cells is sufficient for HBC activation to multipotency. By expression analysis, next-generation sequencing, and immunohistochemical examination, down-regulation of Notch pathway signaling is coincident with HBC activation. Therefore, using HBC-specific conditional knockout of Notch receptors and overexpression of N1ICD, we show that Notch signaling maintains p63 levels and HBC dormancy, in contrast to its suppression of p63 expression in other tissues. Additionally, Notch1, but not Notch2, is required to maintain HBC dormancy after selective neuronal degeneration. Taken together, our data indicate that the activation of HBCs observed after tissue injury or sustentacular cell ablation is caused by the reduction/elimination of Notch signaling on HBCs; elimination of Jagged1 expressed by sustentacular cells may be the ligand responsible.
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