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.

Discoidin domain receptor 2 controls craniofacial morphology by acting in skeletal progenitor cells and chondrocytes to control collagen matrix organization, chondrocyte polarity, and growth.

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.

Foxc1 proteins prepare the genomes of neural crest-derived cells to facilitate their later development into the cartilages that support the embryonic face.

Sequential live imaging of abnormal skull bone fusion in zebrafish reveals a deeply conserved role of two transcription factors, Twist1 and Tcf12, in regulating stem cell activity during growth of the skull.

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.

Multivariate genotype-phenotype mapping enables quantification of pathway and process-level effects on complex phenotypes and predicts phenotypic effects of novel mutations.

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.

SHH signaling acts through FOXF1/2 transcription factors and antagonizes BMP signaling to specify oral fate and pattern the oral-aboral axis of the mandibular arch to ensure proper formation of jaws.

Spatially distinct ectodermal Wnt and endodermal Shh signals serve to polarize the skate gill skeleton.