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TISSUE-SPECIFIC STEM CELLS |
aDifferentiation and Transcription Laboratory, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia;
bDepartment of Pharmaceutical Biology, Monash University, Parkville, Victoria, Australia;
cHoward Florey Institute, Parkville, Victoria, Australia;
dCentre for Neuroscience, University of Melbourne, Parkville, Victoria, Australia;
eDepartment of Physiology, Monash University, Clayton, Victoria, Australia;
fInstitute for Biomedical Research, Birmingham University, Birmingham, United Kingdom
Key Words. Neural stem cells • c-Myb • Ependymal cells • Transcription factor • Mice
Correspondence: Correspondence: Theo Mantamadiotis, Ph.D., Department of Pharmaceutical Biology, Victorian College of Pharmacy, Monash University (Parkville Campus), 381 Royal Parade, Parkville, Victoria 3052, Australia. Telephone: 61-3-9903-9574; Fax: 61-3-9903-9638; e-mail: Theo.Mantamadiotis{at}vcp.monash.edu.au
Received on April 22, 2007;
accepted for publication on September 18, 2007.
Disclosure of potential conflicts of interest is found at the end of this article.
First published online in STEM CELLS EXPRESS September 27, 2007.
Ongoing production of neurons in adult brain is restricted to specialized neurogenic niches. Deregulated expression of genes controlling homeostasis of neural progenitor cell division and/or their microenvironment underpins a spectrum of brain pathologies. Using conditional gene deletion, we show that the proto-oncogene c-myb regulates neural progenitor cell proliferation and maintains ependymal cell integrity in mice. These two cellular compartments constitute the neurogenic niche in the adult brain. Brains devoid of c-Myb showed enlarged ventricular spaces, ependymal cell abnormalities, and reduced neurogenesis. Neural progenitor cells lacking c-Myb showed a reduced intrinsic proliferative capacity and reduction of Sox-2 and Pax-6 expression. These data point to an important role for c-Myb in the neurogenic niche of the adult brain.
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