ID 6560
File
Authors
Colak, Dilek Helmhotz Center Munich, German Research Center for Environmental Health, Institute for Stem Cell Research
Mori, Tetsuji Helmhotz Center Munich, German Research Center for Environmental Health, Institute for Stem Cell Research Researchers DB KAKEN
S. Brill, Monika Helmhotz Center Munich, German Research Center for Environmental Health, Institute for Stem Cell Research / Physiological Genomics, University of Munich
Pfeifer, Alexander Institute for Pharmacology and Toxicology, University of Bonn
Falk, Sven Institute of Anatomy, University of Zurich
Deng, Chuxia Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health
Monteiro, Rui Developmental Biology, Hubrecht Institute
Mummery, Christine Developmental Biology, Hubrecht Institute
Sommer, Lukas Institute of Anatomy, University of Zurich
Götz, Magdalena Helmhotz Center Munich, German Research Center for Environmental Health, Institute for Stem Cell Research / Physiological Genomics, University of Munich
Keywords
neural stem cells
Olig2
Dlx2
neurogenesis
oligodendrocytes
transplantation
Abstract
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.
Publisher
Society for Neuroscience
Content Type
Journal Article
Link
ISSN
02706474
NCID
AA10620404
Journal Title
The Journal of Neuroscience
Current Journal Title
The Journal of Neuroscience
Volume
28
Issue
2
Start Page
434
End Page
445
Journal Section
Development/Plasticity/Repair
Published Date
2008-01-09
Publisher-DOI
Text Version
Publisher
Rights
Copyright © 2008 Society for Neuroscience
Citation
Colak, Dilek, et al. "Adult neurogenesis requires Smad4-mediated bone morphogenic protein signaling in stem cells." Journal of Neuroscience 28.2 (2008): 434-446.
Department
Faculty of Medicine/Graduate School of Medical Sciences/University Hospital
Language
English