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Increased Integration in Mutant Mice: An Analysis of the Patterns of Covariance through Ontogeny in Fgfr2 Mice

Mutations in the FGF/FGFR2 gene result in the premature fusion of fibrous and cartilaginous joints in the skull. This results in profound morphological changes in the skulls of both humans and mice with these mutations. Previous studies have indicated that morphological integration of the skull is expected to become more pronounced in dysmorphic syndromes, including FGFR2 syndromes which result in craniosynostosis. In this study, our objective was to test two hypotheses: 1) that the magnitude of morphological integration was greater in Fgfr2C342Y/+ mutant mice relative to wild‐type littermates; and 2) that the magnitude of morphological integration would increase through ontogeny.