Notch2 signaling maintains NSC quiescence in the murine ventricular-subventricular zone
Open accessAbstract
Neurogenesis continues in the ventricular-subventricular zone (V-SVZ) of the adult forebrain from quiescent neural stem cells (NSCs). V-SVZ NSCs are a reservoir for new olfactory bulb (OB) neurons that migrate through the rostral migratory stream (RMS). To generate neurons, V-SVZ NSCs need to activate and enter the cell cycle. The mechanisms underlying NSC transition from quiescence to activity are poorly understood. We show that Notch2, but not Notch1, signaling conveys quiescence to V-SVZ NSCs by repressing cell-cycle-related genes and neurogenesis. Loss of Notch2 activates quiescent NSCs, which proliferate and generate new neurons of the OB lineage. Notch2 deficiency results in accelerated V-SVZ NSC exhaustion and an aging-like phenotype. Simultaneous loss of Notch1 and Notch2 resembled the total loss of Rbpj-mediated canonical Notch signaling; thus, Notch2 functions are not compensated in NSCs, and Notch2 is indispensable for the maintenance of NSC quiescence in the adult V-SVZ.
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Fgfr and Notch signaling and oxidative phosphorylation showed lateral wall and male enrichment.
“Several molecular and metabolic processes important for stem cell self-renewal, maintenance, and proliferation, such as Fgfr and Notch signaling and oxidative phosphorylation, showed lateral wall and male enrichment (Engler et al., 2018; Kawai et al., 2017; Llorens-Bobadilla et al., 2015; Zheng et al., 2004).”
From Single-Cell Analysis of Regional Differences in Adult V-SVZ Neural Stem Cell Lineages (2019) · cites this paper as Engler et al., 2018
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- Authors
- Engler, A., Rolando, C., Giachino, C., Saotome, I., Erni, A., Brien, C., Zhang, R., Zimber-Strobl, U., Radtke, F., Artavanis-Tsakonas, S., Louvi, A., & Taylor, V.
- Affiliations
- University of Basel (CH)
- Yale University (US)
- École Polytechnique Fédérale de Lausanne (CH)
- Corresponding author
- Taylor, Verdon
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2018-01
- Volume
- 22
- Issue
- 4
- Pages
- 992-1002
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2784635738
- Cited by
- 125
- References
- 42
- Citations by year
- 2026: 8 · 2025: 14 · 2024: 14 · 2023: 13 · 2022: 18 · 2021: 17 · 2020: 21 · 2019: 14 · 2018: 6
- FWCI
- 5.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, cc-by-nc-nd)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Site cant be reached (submittedVersion, cc-by-nc-nd)
- Funders
- Swiss National Science Foundation (310030_143767)
- University of Basel
- Forschungsfonds University of Basel
- Biogen
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- Notch2 signaling, Notch1, neural stem cell quiescence, ventricular-subventricular zone, rostral migratory stream, olfactory bulb neurogenesis, cell cycle re-entry, RBPJ, Notch signaling, adult neurogenesis, stem cell exhaustion
- MeSH terms
- Animals, Cell Differentiation, Signal Transduction, Lateral Ventricles, Mice, Receptor, Notch2, Neural Stem Cells
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