Fig. 3. Decreased Gli activator function and/or increased Gli repressor function represses ectopic Hh target gene expression in igu embryos. (A-I) Introduction of dtr/gli1 mutant alleles into the igu genetic background suppressed ectopic Hh target gene expressions in somites. In dtr/gli1^–/– embryos (A-C), the expression of nk2.2 and ptc1 is reduced, but en1 expression is normal. In dtr/gli1^–/+;igu^–/– embryos (D-F), nk2.2 expression is similar to dtr/gli1^–/– embryos (D), with no nk2.2 expression in the posterior neural tube. By contrast, the expression of en1 (E) and ptc1 (F) are similar to that seen in igu^–/– mutants; however, en1 expression is reduced in anterior somites. In dtr/gli1^–/–;igu^–/– embryos (G-I), the decrease of en1 and ptc1 is more evident (H,I), and the overall phenotype including nk2.2 (G) is stronger than in dtr/gli1^–/– embryos. Insets show higher magnification views of ptc1 expression in the trunk region. (J-O) A drastic reduction of Hh target gene expression is caused by the introduction of a yot/gli2 mutant allele into the igu genetic background. One copy of yot/gli2 completely suppressed ectopic target gene expression (M-O), and the resulting phenotype is similar to or even stronger than that seen in yot/gli2^–/– embryos (J-L). An arrowhead marks a spot of nk2.2 expression, which is consistently seen only in yot/gli2^–/– embryos (J) but not in yot/gli2^–/+;igu^–/– embryos (M). The genotypes of these embryos were confirmed by PCR after in situ staining.