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. Author manuscript; available in PMC: 2009 Mar 10.
Published in final edited form as: Curr Top Dev Biol. 2008;85:225–260. doi: 10.1016/S0070-2153(08)00809-0

Figure 4. Many IFT mutations cause polydactyly and loss of ventral neural tube fates.

Figure 4

(A) In embryos lacking IFT components such as IFT88, IFT172 and Kif3a, a gradient of Shh is established, but signaling through Gli2-Act and formation of Gli3-Rep are disrupted. Consequently, these mutants do not properly activate the Hh transcriptional targets, and display loss of ventral cell types (FP, V3, MN) and expansion of more dorsal subtypes (V0, V1, V2) in the neural tube. In IFT mutant limb buds, disruption of Gli3-Rep formation leads to polydactyly. (B) In contrast to other IFT mutants, THM1 mutants display increased Hh signaling mediated by Gli2-Act and Gli3-Act, leading to an increase in ventral subtypes (FP, V3, MN) in the neural tube. THM1 is also essential for Gli3 processing, defects of which in THM1 mutants result in polydactyly.