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Fig. 6. Reduced FGF signaling in En1 mutant calvariae. (A)
Expression of Fgfr1, Fgfr2 and Fgf18 in the coronal suture,
and the parietal and frontal bones, at P1. Fgfr1, Fgfr2 and
Fgf18 are co-expressed by ectocranial periosteal osteoblasts in the
parietal and frontal bones. Fgfr1 is absent from wild-type sutural
osteprogenitors, whereas Fgfr2 and Fgf18 are expressed at
these locations. In En1 mutants, Fgfr1 and Fgfr2
are upregulated in the sutural mesenchyme (arrowheads indicate the parietal
and frontal bone margins). (B) Northern blot analysis of Fgfr1
and Fgfr2 expression during the differentiation of cultured primary
calvarial osteoblasts. Relative to Gapdh, no significant differences
in Fgfr1 or Fgfr2 levels were observed in wild-type and
En1-/- osteoblasts. (C) Loss of Spry2
expression in the calvarial osteoblasts (arrow) and osteoprogenitors
(arrowheads) of En1 mutants. (D) Expression of pERK in
calvarial bones of wild-type and En1-/- mice at P1. pERK
displays strong activity in wild-type endosteal osteoblasts lining the frontal
bone trabeculae, but is only weakly present at the osteogenic fronts
(arrowheads), and is absent from ectoperiosteal osteoblasts (arrow).
En1 mutants display severely reduced pERK in endosteal osteoblasts.
p, parietal bone; f, frontal bone. (E) Proposed model
for the interactions between EN1 and FGF signaling events during calvarial
osteogenesis. The calvarial bone is postulated to divide into spatial
subdomains (sutural osteoprogenitors, ectoperiosteal osteoblasts, endosteal
osteoblasts) that respond differentially to FGF signaling. Scale bars: 0.2 mm
in A; 0.1 mm in C; 0.1 mm in D.
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