The ability of cartilaginous fishes to generate new cartilage through adulthood, and to spontaneously repair damaged cartilage, could shed light on novel cell-based therapies for cartilage injury in mammals.

In addition to a neural crest cell specific role, AP-2α and AP-2ß cooperatively promote craniofacial development through regulating chromatin and gene expression dynamics in the facial surface ectoderm.

The brain and olfactory epithelium play a key role in pattering chondrogenic areas in the developing face, which is partly based on the release of SHH from neurosensory structures into the facial mesenchyme.

The clonal oriented cell dynamics enables directional expansion and accurate scaling of sheet-like or rod-like cartilaginous elements and uncouples the mechanisms of elongation from thickness or diameter control.

Analysis of 3D reconstructions of chondrocrania of the Fgfrc^C342Y/+ Crouzon syndrome mouse show the direct effects of this Fgfr2 mutation on embryonic cranial cartilage formation and the indirect effects of chondrocranial morphology on cranial dermal bone development.