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Fig. 1 gpc4 mRNA fails to rescue craniofacial cartilage morphology of gpc4-/- (knypek) embryos. A-D: Ventral view of zebrafish pharyngeal arch cartilages stained with Alcian Blue at 7 days post-fertilization (dpf). Compared to wild-type siblings (A), the palatoquadrate, ceratohyal, and symplectic cartilages of gpc4-/- larvae were shorter and thicker (B). Wild type siblings injected with synthetic gpc4 mRNA developed normally (C). Injection of the same dose of synthetic mRNA fully rescued gastrulation defects of gpc4-/- embryos (Topczewski et al. [2001]), but the mutant cartilage phenotype was not suppressed (D). E-H: Ventral view of isolated larval neurocrania (7 dpf). Compared to wild types (E), the anterior ethmoid plate (ep) of gpc4-/- mutant larvae was shortened and the trabeculae (tr) were farther apart, causing an enlarged hypophyseal fenestra (hpf) (F). The posterior parachordal plate (pch) was relatively normal. Wild type siblings injected with synthetic gpc4 mRNA developed normal neurocrania (G), but in injected mutants the neurocranial defect was not suppressed (H). I-K: Flat-mounted hyosymplectic cartilages (7 dpf). Compared to wild types (I), gpc4-/- larvae showed a severely shortened symplectic region (sy, J). The hyomandibular region (hm) was less affected. This defect in gpc4-/- larvae was not suppressed by gpc4 mRNA injection (K). L-N: Flat-mounted ceratohyal cartilages (7 dpf). The ceratohyal of a wild type embryo (L) is much longer than that of a gpc4-/- embryo (M). The failure of ceratohyal cartilage elongation is not suppressed by injecting gpc4 mRNA into a gpc4-/- embryo (N). ch, ceratohyal; ep, ethmoid plate; hm, hyomandibular; hpf, hypopophyseal fenestra; hs, hyosymplectic; m, Meckel′s cartilage; pch, parachordal plate; pq, palatoquadrate; sy, symplectic; tr, trabeculae.