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Fig. 7. A model for Gli-mediated Shh target gene induction in the somite. (A) In wild type, Shh signaling modifies Gli2 into a strong activator, Gli2A, to activate target genes, including Gli1. Gli1 acts secondarily to activate Ptch and Hhip. In the absence of Shh, or when overexpressed, Gli3 acts as a repressor, Gli3R. In Gli2^–/– and Gli2^–/–Gli3^+/–, an activator function of Gli3 is revealed (in blue), to compensate for loss of Gli2. In Gli3^–/– and Gli2^+/–Gli3^–/–, a repressor function of Gli2 is revealed (in blue), to compensate for loss of Gli3. In wild-type embryos Gli2R and Gli3A may be present but play minor roles. This possibility is not illustrated for simplicity. In Gli2^–/–Gli3^–/– embryos, both activator and repressor functions of Gli2 and Gli3 are lost resulting in a low level of Shh-independent expression of target genes. The low level of Gli1 in these embryos is non-functional (X). (B) The diagram illustrates somite morphology and gene expression in wild type and Gli mutants. Somite patterning and gene expression is largely normal in Gli2^–/–, Gli3^–/– and Gli2^–/–Gli3^+/– embryos (left). In Gli2^–/–Gli3^–/– embryos, there is ventromedial expansion of Pax3-positive cells (Pax3⁺), mixing of Pax1⁺ and Myf5⁺ cells, and expression of Myf5 in the medial lip is lost (right).

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