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Concurrent inactivation of ptc1 and ptc2 results in severe developmental defects. At 18 hpf, a somite phenotype becomes apparent in the ptc1;ptc2 double mutants, where the chevron shaped form of the somites becomes straight (A,B), which is a typical consequence of increased activity of the Hh pathway. At 24 hpf, ptc1;ptc2 double mutants do not develop a lens but the primitive eye field is still present (C,D). At 48 hpf the eyes are completely absent. Additionally, reduced pigmentation, an absence of the nose, and an underdeveloped ear can be observed at 48 hpf (E,F). Expression levels of nkx2.2a confirms that the pathway becomes more activated upon losing wild type alleles of ptc1 or ptc2, with the highest expression in the ptc1;ptc2 mutant, mainly in the anterior brain structures (G-J).
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