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.