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Vol. 16, No. 24, pp. 3173-3185, December 15, 2002
/ mice
1 Gene Center and Institute of Biochemistry, University of
Munich, 81377 Munich, Germany; 2 Institute of Molecular
Biology, Austrian Academy of Sciences, 5020 Salzburg, Austria
Lymphoid enhancer factor (LEF1), a nuclear mediator of Wnt
signaling, is required for the formation of organs that depend on
inductive interactions between epithelial and mesenchymal tissues. In
previous tissue recombination experiments with normal and
Lef1
/ tooth germs, we found that the effect
of LEF1 expression in the epithelium is tissue nonautonomous and
transferred to the subjacent mesenchyme. Here we examine the molecular
basis for LEF1 function and find that the epithelium of the
developmentally arrested Lef1/ tooth
rudiments fails to express Fgf4, Shh, and
Bmp4, but not Wnt10a. We identify the
Fgf4 gene as a direct transcriptional target for LEF1 and
show that beads soaked with recombinant FGF4 protein can fully overcome
the developmental arrest of Lef1/ tooth
germs. In addition, we find that FGF4 beads induce rapidly the
expression of Fgf3 in dental mesenchyme and that both
epithelial and mesenchymal FGF proteins induce the delayed expression
of Shh in the epithelium. Taken together, these data
indicate that a single target of LEF1 can account for the function of
LEF1 in tooth development and for a relay of a Wnt signal reception to a cascade of FGF signaling activities, allowing for a sequential and
reciprocal communication between epithelium and mesenchyme.
[Key Words: LEF1; Wnt; FGF; epithelial-mesenchymal interactions]
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