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Fig. 3. Analysis of Ptch1 and ß-catenin mutant
skeletons. (A) Skeletal preparations of 16.5 dpc mouse embryos. A
forelimb of each embryo is shown in the lower panel. The posterior skull in
the Ptch1c/-; Col2a1-Cre mutant did not form (arrow).
Skull formation in the Ptch1c/-; Catnbc/-;
Col2a1-Cre double mutant was rescued (arrow). Mineralization (arrows,
lower panel) in the long bones was more severely reduced in the
Ptch1c/-; Catnbc/-; Col2a1-Cre double mutant
than in either of the single mutants. S, scapular; H, humerus; R, radius; U,
ulna. (B) ß-catenin is not required for Ihh signaling. Consecutive
sections of the developing humerus at 14.5 dpc were examined by in situ
hybridization with the indicated 35S-labelled riboprobes. In both
Ptch1c/-; Col2a1-Cre and Ptch1c/-;
Catnbc/-; Col2a1-Cre mutant embryos, expression of the Hh
signaling targets Hip1 and Gli1, and of Pthrp, was
similarly upregulated in cartilage, perichondrium and joints (arrows). The
perichondrium was slightly thinner in the Ptch1c/-;
Catnbc/-; Col2a1-Cre mutant than in the
Ptch1c/-; Col2a1-Cre mutant.