Keeping Them Quiet: BMPs Maintain Adult Neural Stem Cell Quiescence Mantissa A. Johnston, Daniel A. Lim  Cell Stem Cell  Volume 7, Issue 1, Pages 9-10 (July 2010) DOI: 10.1016/j.stem.2010.06.006 Copyright © 2010 Elsevier Inc. Terms and Conditions

Figure 1 Model of BMP Regulation of Neural Stem Cell Quiescence in the Adult Dentate Gyrus In the subgranular zone (SGZ), there is a population of radial, Sox2+ neural stem cells (NSCs) in both quiescent (purple cell, red nucleus) as well as actively dividing states (purple cell, green nucleus). In this model, antagonism of BMP signaling causes quiescent NSCs to enter the cell cycle (straight left-to right arrow), whereas BMPs induce the quiescent state (right to left arrow). Proliferative NSCs give rise to more rapidly dividing progenitors (dark blue, nonradial cell) that later migrate into the granule cell layer (GCL, light-blue cells) and differentiate into postmitotic neurons (red cell). In this model, BMP signaling through the BMPR-IA receptor induces a “quiescence program” in SGZ NSCs, allowing for cell cycle re-entry even after prolonged G0 arrest. When bound by BMP, BMPR-IA becomes activated and phorphorylates SMAD1, which then translocates into the nucleus, activating target genes. Nondividing SGZ NSCs have both BMPR-IA and P-SMAD1 (left inset) and presumably a BMP-dependent program for quiescence. Actively dividing, Sox2+ NSCs do not have P-SMAD1. For cell cycle re-entry from quiescence, BMP signaling may need to be downregulated, possibly by BMP antagonists such as Noggin (right inset). Cell Stem Cell 2010 7, 9-10DOI: (10.1016/j.stem.2010.06.006) Copyright © 2010 Elsevier Inc. Terms and Conditions