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Fig. 6. BMPs regulate morphology and are necessary and sufficient for the
cell-cycle exit of GFAP-expressing cells in vivo. Transgenic animals
overexpressing BMP4 or noggin were analyzed at P15. (A-K) Immunofluorescence
for GFAP and Ki67 in the hippocampus SGZ (A-D) and ML (E-K). (L) Plot of
Ki67+GFAP+ cells in the SGZ
(*P<0.03) and the ML (*P<0.01,
**P<0.04). (M) Average number of processes per
GFAP+ cell. Numbers in parentheses indicate the number of cells
analyzed. *P<0.01, **P<0.001
ANOVA. (A,B,L) GFAP-expressing cells in the SGZ remain in cell cycle and are
increased in number when noggin is overexpressed. Arrows indicate clusters of
Ki67+ cells. (C,L) Overexpression of BMP4 in the SGZ promotes
cell-cycle exit of GFAP+ cells. (D) High magnification confocal
image demonstrating co-localization of Ki67 and GFAP in the SGZ of noggin
mice. (F,G,L) Few GFAP-expressing cells in the ML remain in cell cycle in
wild-type or BMP4-overexpressing mice. (E,L) BMP inhibition in the ML
maintains GFAP+ cells in cell cycle. Arrows (E) indicate
Ki67+GFAP+ cells. (H) High magnification confocal image
demonstrating co-localization of Ki67 and GFAP in the ML of noggin mice.
(J,K,M) GFAP+ cells in the ML exhibit branched morphologies that
become further ramified with BMP4 overexpression. (I,M) Noggin overexpression
in the ML prevents the formation of stellate morphology, and these cells
resemble the thin elongated GFAP+ cells in the SGZ (H,D). GCL,
granule cell layer; SGZ, subgranular zone; h, hilus; ML, molecular layer; WT,
wild type; NN, NSE-Noggin; NB, NSE-BMP4. Scale bar in B: 20 µm for A-C,E-G;
10 µm for D,H-K.
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