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Open Access Green as soon as Postprint is submitted to ZB.
Adult neurogenesis requires Smad4-mediated bone morphogenic protein signaling in stem cells.
J. Neurosci. 28, 434-445 (2008)
In the mammalian brain, neurogenesis continues only in few regions of the forebrain. The molecular signals governing neurogenesis in these unique neurogenic niches, however, are still ill defined. Here, we show that bone morphogenic protein (BMP)-mediated signaling is active in adult neural stem cells and is crucial to initiate the neurogenic lineage in the adult mouse subependymal zone. Conditional deletion of Smad4 in adult neural stem cells severely impairs neurogenesis, and this is phenocopied by infusion of Noggin, an extracellular antagonist of BMP. Smad4 deletion in stem, but not progenitor cells, as well as Noggin infusion lead to an increased number of Olig2-expressing progeny that migrate to the corpus callosum and differentiate into oligodendrocytes. Transplantation experiments further verified the cell-autonomous nature of this phenotype. Thus, BMP-mediated signaling via Smad4 is required to initiate neurogenesis from adult neural stem cells and suppress the alternative fate of oligodendrogliogenesis
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
neural stem cells; Olig2; Dlx2; neurogenesis; oligodendrocytes; transplantation
ISSN (print) / ISBN
0270-6474
e-ISSN
1529-2401
Journal
Journal of Neuroscience
Quellenangaben
Volume: 28,
Issue: 2,
Pages: 434-445
Publisher
Society for Neuroscience
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Stem Cell Research (ISF)