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Pax  genes have been shown to play important roles in mammalian development and organogenesis.  Pax9,  a member of this transcription factor family, is expressed in somites, pharyngeal pouches, mesenchyme involved in craniofacial, tooth, and limb development, as well as other sites during mouse embryogenesis. To analyze its function in vivo, we generated  Pax9  deficient mice and show that  Pax9  is essential for the development of a variety of organs and skeletal elements. Homozygous  Pax9 -mutant mice die shortly after birth, most likely as a consequence of a cleft secondary palate. They lack a thymus, parathyroid glands, and ultimobranchial bodies, organs which are derived from the pharyngeal pouches. In all limbs, a supernumerary preaxial digit is formed, but the flexor of the hindlimb toes is missing. Furthermore, craniofacial and visceral skeletogenesis is disturbed, and all teeth are absent. In Pax9 -deficient embryos tooth development is arrested at the bud stage. At this stage,  Pax9  is required for the mesenchymal expression of  Bmp4, Msx1,  and  Lef1,  suggesting a role for  Pax9  in the establishment of the inductive capacity of the tooth mesenchyme. In summary, our analysis shows that  Pax9  is a key regulator during the development of a wide range of organ primordia.

Pax9-deficient mice lack pharyngeal pouch derivatives and teeth and exhibit craniofacial and limb abnormalities