Fig. 9

Effects of SHH and FGF signal inhibitors on cartilage formation. a–f, dorsal (a–c) and ventral (d–f) views of control (a, d), cyclopamine-treated (b, e), and SU5402-treated (c, f) embryos at 5 dpf. Inhibition of SHH caused malformation of trabecular (tr), parachordal (pa), Meckel’s (me), and ceratohyal (ch) cartilages (b, e). Inhibition of FGFs causes malformation of ceratohyal cartilage (ch), while other craniofacial cartilages appear unaffected (c, f). g–l, dorsal (g–i) and ventral (j–l) views of control (g, j), cyclopamine-treated (h, k), and SU5402-treated (i, l) embryos at 5 dpf. Cartilages in maxillary (g–i) and mandibular (j–l) barbels were visualized by Alcian blue. The cartilages of cyclopamine-treated embryos entered into the maxillary barbel and extended to the tip of the barbel, consistent with the control group (h), although they became thinner compared with the controls (g). In the mandibular region, the barbel cartilage was absent in cyclopamine-treaed group (k). FGF inhibition caused reduction in cartilage length in the maxillary barbel (arrowhead in i). In the mandibular region, barbel cartilages were severely reduced (l). amdb, anterior mandibular barbel; ch, ceratohyal cartilage; me, Meckel’s cartilage; mxb, maxillary barbel; pa, parachordal cartilage; pmdb, posterior mandibular barbel; tr, trabecular cartilage. Anterior is the upper side in all images and the proximal side is left in g–l. Scale bars in a–i are 500 μm and 200 μm in j–l