Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-12080
Colak, D; Mori , T; Brill, M; Pfeifer, A; Falk, S; Deng, C; Monteiro, M; Mommery, C; Sommer, L; Götz, M (2008). Adult neurogenesis requires Smad4-mediated bone morphogenic protein signaling in stem cells. Journal of Neuroscience, 283(2):434-446.
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.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Institute of Anatomy|
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Deposited On:||03 Feb 2009 09:27|
|Last Modified:||28 Nov 2013 01:32|
|Publisher:||Society for Neuroscience|
|Additional Information:||Holder of copyright: The Society for Neuroscience|
|Citations:||Web of Science®. Times cited: 106|
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