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Nat. Neurosci. 9, 1099-1107 (2006)
Stem cell persistence into adulthood requires self-renewal from early developmental stages. In the developing mouse brain, only apical progenitors located at the ventricle are self-renewing, whereas basal progenitors gradually deplete. However, nothing is known about the mechanisms regulating the fundamental difference between these progenitors. Here we show that the conditional deletion of the small Rho-GTPase cdc42 at different stages of neurogenesis in mouse telencephalon results in an immediate increase in basal mitoses. Whereas cdc42-deficient progenitors have normal cell cycle length, orientation of cell division and basement membrane contact, the apical location of the Par complex and adherens junctions are gradually lost, leading to an increasing failure of apically directed interkinetic nuclear migration. These cells then undergo mitoses at basal positions and acquire the fate of basal progenitors. Thus, cdc42 has a crucial role at the apical pole of progenitors, thereby regulating the position of mitoses and cell fate.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
CELL-CYCLE; NEUROEPITHELIAL CELLS; SUBVENTRICULAR ZONE; RADIAL GLIA; ASYMMETRIC DISTRIBUTION; ADHERENS JUNCTIONS; BRAIN-DEVELOPMENT; LAYER NEURONS; BETA-CATENIN; MOUSE-BRAIN
Language
english
Publication Year
2006
HGF-reported in Year
0
ISSN (print) / ISBN
1097-6256
e-ISSN
1546-1726
Journal
Nature Neuroscience
Quellenangaben
Volume: 9,
Issue: 9,
Pages: 1099-1107
Publisher
Nature Publishing Group
Reviewing status
Peer reviewed
Institute(s)
Institute of Stem Cell Research (ISF)
POF-Topic(s)
30204 - Cell Programming and Repair
Research field(s)
Stem Cell and Neuroscience
PSP Element(s)
G-500800-001
PubMed ID
16892058
DOI
10.1038/nn1744
WOS ID
000240080800010
Scopus ID
33748099126
Erfassungsdatum
2006-12-31