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The pharyngeal pouches are a series of epithelial outgrowths of the foregut endoderm. Pharyngeal pouches segment precursors of the vertebrate face into pharyngeal arches and pattern the facial skeleton. These pouches fail to develop normally in zebrafish foxi1 mutants, yet the role Foxi1 plays in pouch development remains to be determined. Here we show that ectodermal Foxi1 acts downstream of Fgf8a during the late stage of pouch development to promote rearrangement of pouch-forming cells into bilayers. During this phase, foxi1 and wnt4a are coexpressed in the facial ectoderm and their expression is expanded in fgf8a mutants. foxi1 expression is unaffected in wnt4a mutants; conversely, ectodermal wnt4a expression is abolished in foxi1 mutants. Consistent with this, foxi1 mutant pouch and facial skeletal defects resemble those of wnt4a mutants. These findings suggest that ectodermal Foxi1 mediates late-stage pouch morphogenesis through wnt4a expression. We therefore propose that Fox1 activation of Wnt4a in the ectoderm signals the epithelial stabilization of pouch-forming cells during late-stage of pouch morphogenesis.

Nanos proteins are essential for developing primordial germ cells (PGCs) in both invertebrates and vertebrates. In invertebrates, also contribute to the patterning of the anterior-posterior axis of the embryo and the neural development. In vertebrates, however, besides the role of Nanos proteins in PGC development, the biological functions of the proteins in normal development have not yet been identified. Here, we analyzed the expression and function of nanos1 during craniofacial development in zebrafish. nanos1 was expressed in the pharyngeal endoderm and endodermal pouches essential for the development of facial skeletons and endocrine glands in the vertebrate head. However, no craniofacial defects, such as abnormal pouches, hypoplasia of the thymus, malformed facial skeletons, have been found in nanos1 knockout animals. The normal craniofacial development of nanos1 knockout animals is unlikely a consequence of the genetic redundancy of Nanos1 with Nanos2 or Nanos3 or a result of the genetic compensation for the loss of Nanos1 by Nanos2 or Nanos3 because the expression of nanos2 and nanos3 was rarely seen in the pharyngeal endoderm and endodermal pouches in wild-type and nanos1 mutant animals during craniofacial development. Our findings suggest that nanos1 expression in the pharyngeal endoderm might be dispensable for craniofacial development in zebrafish.