QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

Help viewing high resolution images Return to article

Fig. 7. TGFß stimulates CNC proliferation while FGF signals downstream of TGFß in mediating cell proliferation during frontal bone development. (A,D) E16.5 calvarial primordium treated with BSA bead for 1 day shows normal growth of the CNC and activity of cell proliferation, as demonstrated by BrdU labeling (D, arrow). (B,E) TGFß1 treatment results in substantial increase in tissue thickness (B, arrow) and cell proliferation (E, arrow) in the E16.5+1 cultured explant. (C,F) Similarly, TGFß2 treatment also results in expansion of frontal bone primordium (C, arrow) and increase in cell proliferation (F, arrow). (G) E14.5 frontal bone primordium treated with BSA beads for 1 day shows normal level of Fgfr2 expression (arrow), as indicated by whole-mount in situ hybridization analysis (dark purple indicates a positive signal). (H) TGFß1 beads induce elevated expression of Fgfr2 (arrows) in the frontal primordium. (I) E14.5 Tgfbr2^fl/fl;Wnt1-Cre mutant frontal bone primordium treated with BSA bead shows very little tissue growth (outlined) and reduced cell proliferation activity (BrdU positive cells in red). (J) E14.5 Tgfbr2^fl/fl;Wnt1-Cre mutant frontal bone primordium treated with FGF2 bead shows extensive increase in tissue growth (outlined) and restored cell proliferation activity (arrows). (K) E14.5 Tgfbr2^fl/fl;Wnt1-Cre mutant parietal bone primordium explant treated with BSA beads (left side) for 1 day shows basal level of Fgfr2 expression, while TGFß beads treatment (right side) shows strongly induced Fgfr2 expression (arrows, dark brown). None of the explants contains dura matter or epithelium. Scale bars: 100 µm.

Return to article