The Journal of Neuroscience, January 25, 2006, ():
Loss of p53 Induces Changes in the Behavior of Subventricular Zone Cells: Implication for the Genesis of Glial Tumors
J. Neurosci. Gil-Perotin et al.
26: 1107
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplemental figure. Model of the changes induced by p53 loss of
function in the adult SVZ. On the left, within the boxed area, the
anatomical region that is schematically shown in the diagram is
indicated (v= lateral ventricle). In wild type mice, the SVZ is
composed of large migratory chains of neuroblasts (red) within tunnels
composed of GFAP+ cells (blue). C cells (green) are fast-proliferating
cells sparse within the chains. GFAP+ B cells are relatively quiescent,
while C cells are the fast-proliferating compartment and are the
precursors for A neuroblasts. In the presence of p53, the number of
cells in each population is determined by an equilibrium between
generation (due to self-renewal and/or proliferation) and elimination
(due to apoptotic death or lineage progression). In the absence of p53,
however, there is a growth advantage of the slow and fast proliferating
compartment and rapid differentiation into neuroblasts, thus resulting
in the formation of clusters of A and B cells. These changes are
partially compensated by increased cell death. The association of Ras
activation or ENU exposure with the loss of p53 induces an increase of C
cells, due to the recruitment of slow proliferating cells into this
rapidly expanding compartment and impaired differentiation. These
changes create the substrate for the genesis of periventricular
glioblastomas.
