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. Author manuscript; available in PMC: 2008 Aug 15.
Published in final edited form as: Dev Biol. 2007 May 31;308(2):343–354. doi: 10.1016/j.ydbio.2007.05.030

Figure 5.

Figure 5

A conditional knockout of Shh by the Shhgfpcre causes a continuous low level of Shh signaling throughout limb development. Shh expression expands after eight hours of cyclopamine treatment (A) compared to control forelimbs (B) due to Shh autoregulation. Likewise, a greater amount of the forelimb mesenchyme has attempted to upregulate Shh at E12.5 in Shh nulls (C) than in wildtype (D). At E10.5, Shhgfpcre/Shhc forelimbs (F) have reduced levels of Shh, compared to wildtype forelimbs (E). At E11.5 Shh is still expressed, albeit at low levels (arrowhead), in Shhgfpcre/Shhc forelimbs (H) in a domain proximal and anterior to the Shh domain in wildtype forelimbs (G). Shh signaling, as indicated by Ptc1 expression, is significantly reduced in E10.5 Shhgfpcre/Shhc forelimbs (J) compared to wildtype forelimbs (I). At E11.5, only extremely faint Ptc expression can be observed in E11.5 Shhgfpcre/Shhc forelimbs (K) compared to wildtype forelimbs (L).