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Notch2 signaling maintains NSC quiescence in the murine ventricular-subventricular zone.
Cell Rep. 22, 992-1002 (2018)
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. Using a combinatorial knockout approach, Engler et al. systematically analyze Notch signaling mutants. Their study demonstrates the role of Notch2 in the maintenance of quiescent NSCs in the adult murine brain.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Neural Stem Cells ; Neurogenesis ; Niche ; Notch ; Olfactory Bulb ; Quiescence; Neural Stem-cells; Adult Brain; Neuronal Precursors; Subependymal Zone; Embryonic Origin; Nervous-system; Olfactory-bulb; Self-renewal; Migration; Niche
ISSN (print) / ISBN
2211-1247
e-ISSN
2211-1247
Journal
Cell Reports
Quellenangaben
Volume: 22,
Issue: 4,
Pages: 992-1002
Publisher
Cell Press
Publishing Place
Cambridge
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Research Unit Gene Vector (AGV)