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. Author manuscript; available in PMC: 2009 Sep 15.
Published in final edited form as: Dev Biol. 2008 Jul 9;321(2):407–419. doi: 10.1016/j.ydbio.2008.07.005

Fig. 2.

Fig. 2

Reduced postnatal growth of the caudal neurocranium and the cranial base in Dermo1-Cre;Pkd1 mice. (A) Representative radiograph of control and Dermo1-Cre;Pkd1 skulls (lateral view) shows the dome-shaped neurocranium, a characteristic feature of the Dermo1-Cre;Pkd1 mutant mice. (B) Ventral view of the cranium from 5-days old control and mutant mice. In the Pkd1 knockout mice, an ossified contract is formed in the sphenooccipital synchondrosis (SOS) (arrow) and the presphenoid synchondrosis (PSS) is greatly reduced in size (arrowhead). (C) Alizarin red and Alcian blue staining of the E18.5 skulls demonstrates a wide open basicranial (arrow) and hypophyseal (arrowhead) fenestrae in the mutant cranial base. (D) Premature ossification of the sphenooccipital synchondrosis (arrow) impairs longitudinal growth of the cranial base. Double calcein/alizarin complexon in vivo labelling shows decreased mineralization of the sphenoid and basisphenoid bones (brackets) between P5 and P12. (E) Dorsal view of the skull base from wild type and knockout adult mice reveals a reduced length of the basisphenoid and basioccipital bones (double-headed arrows) in Dermo1-Cre;Pkd1 mice. The presphenoid and sphenooccipital synchondroses are closed in the mutant, whereas they remain patent in control mice. Bo-basioccipital bone, Bs-basisphenoid bone