Cortical Neural Precursors Inhibit Their Own Differentiation via N-Cadherin Maintenance of β-Catenin Signaling

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Developmental Cell (Impact Factor: 9.71). 03/2010; 18(3):472-9. DOI: 10.1016/j.devcel.2009.12.025
Source: PubMed


Little is known about the architecture of cellular microenvironments that support stem and precursor cells during tissue development. Although adult stem cell niches are organized by specialized supporting cells, in the developing cerebral cortex, neural stem/precursor cells reside in a neurogenic niche lacking distinct supporting cells. Here, we find that neural precursors themselves comprise the niche and regulate their own development. Precursor-precursor contact regulates beta-catenin signaling and cell fate. In vivo knockdown of N-cadherin reduces beta-catenin signaling, migration from the niche, and neuronal differentiation in vivo. N-cadherin engagement activates beta-catenin signaling via Akt, suggesting a mechanism through which cells in tissues can regulate their development. These results suggest that neural precursor cell interactions can generate a self-supportive niche to regulate their own number.

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    • "0 ; Franco et al . , 2011 ; Jossin and Cooper , 2011 ; Shikanai et al . , 2011 ; Gartner et al . , 2012 ) . N - cadherin and its effector , β - catenin , are expressed in radial glia cells , where they regulate their proliferation and neurogenesis ( Brault et al . , 2001 ; Machon et al . , 2003 ; Woodhead et al . , 2006 ; Kadowaki et al . , 2007 ; Zhang et al . , 2009 ; Mutch et al . , 2010 ) . Recent findings suggest additional functions of N - cadherin in glial - independent somatic translocation , and glial - guided migration ( Kawauchi et al . , 2010 ; Franco et al . , 2011 ; Jossin and Cooper , 2011 ) . The diverse functions of N - cadherin in the neocortex indicate that its activity must be tig"
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