Developmental and evolutionary significance of the zygomatic bone

The evolution of vertebrate groups, including Homo, is marked by repeated instances of extension and retrusion of the facial skeleton. The exact processes by which these changes occur are unknown but require marked cooperation among developing hard and soft tissues, the cooperation likely driven by genes. Several different mutations in fibroblast growth factor receptors (FGFRs) cause craniosynostosis syndromes, human diseases marked by facial retrusion. 3D morphometric analysis of humans carrying FGFR mutations confirms a correspondence between facial retrusion and causative mutations but the zygoma is relatively less affected than other facial bones depending on the specific mutation. We analyze variation in facial morphology in humans and mice carrying orthologous FGFR mutations, in dogs selected for unusually flat faces, and in a managed colony of captive baboons showing pronounced variation in facial prognathism. Regardless of the source of variation (mutation, selection, normal variation), zygoma morphology remains relatively stable while other bones of the midface change drastically. Whether zygoma morphology represents an adjustment that resists the effects of changes in midfacial architecture while ensuring proper hafting of the facial skeleton onto the neurocranium, and how this adjustment might be accomplished developmentally remain open questions.