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. Author manuscript; available in PMC: 2013 Feb 15.
Published in final edited form as: Dev Biol. 2011 Dec 11;362(2):230–241. doi: 10.1016/j.ydbio.2011.12.010

Figure 7. Model of tissue-tissue interactions during facial skeleton development.

Figure 7

(A) Endodermal Shha induces fgf8a and shha expression in the oral ectoderm. Whereas ectodermal Fgf8a and/or Shha promote the growth and/or differentiation of jaw skeletal precursors, an endoderm-independent Edn1 and Bmp4 signaling center in the aboral ectoderm regulates the DV patterning of jaw precursors. Endoderm may also have direct effects on skeletal growth and/or differentiation.

(B) Schematic of the wild-type arches shows gene expression in the pharyngeal endoderm (red outlines), oral ectoderm (dark blue outlines), and aboral ectoderm (light blue outlines), as well as mandibular- and hyoid-arch-derived cartilage precursors (black outlines with light blue fill) at 36 hpf. fgf8a (green) is expressed within the pitxc2a-positive (grey) oral ectoderm, and bmp4 (orange) and edn1 (blue) are expressed within the aboral ectoderm and pouch endoderm. shha (pink) is expressed in the medial pharyngeal endoderm (and weakly in the oral ectoderm, not shown). Shha signaling (yellow arrow) promotes fgf8a expression, with Fgf8a signaling (red arrow) regulating the position of the lower jaw skeleton.

(C–E) In spns2b1110, s1pr2, and sox32 mutants, disorganization and/or loss of the pharyngeal endoderm results in altered gene expression within the oral and aboral ectoderm. In Class I S1P mutants, altered morphogenesis of Shha-expressing endoderm cells induces ectopic fgf8a expression in the oral ectoderm and the induction of ectopic midline cartilage (dotted line). In class 2 S1P and sox32 mutants, loss of anterior endoderm results in reduction of fgf8a expression, posterior truncation of the oral ectoderm, and loss of jaw skeleton.

(F and G) Transient embryo-wide Shha misexpression (light pink) results in increased Shha signaling (yellow arrowheads), dorsal-lateral displacement of fgf8a and the pitxc2a-expressing oral ectoderm, and the formation of ectopic maxillary cartilage (dotted line). Shha misexpression in sox32 mutants restores fgf8a expression and partially rescues jaw skeleton development.