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Fig. 4. Gli2, but not Gli1, is required for Shh signaling in Ptc mutants. X-gal staining of Ptc-lacZ in six- to eight-somite E8.5 embryos. In wild-type embryos, Ptc-lacZ is expressed in the ventral CNS and somites (A). The expression of Ptc-lacZ is not altered in Gli1zfd/zfd;Ptc+/– embryos (B), but the expression is downregulated in Gli2zfd/zfd;Ptc+/– embryos (C). Loss of Ptc function results in upregulation of Ptc-lacZ throughout the embryos (D). Removal of Gli1 function in Ptc–/– embryos does not rescue the overexpression of Ptc-lacZ (E). However, removal of Gli2 function in Ptc–/– embryos (F) reduces the overexpression of Ptc-lacZ in the head (arrow) and the trunk mesoderm (arrowhead). Scale bar: 0.5 mm.





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