Dynamic morphological changes in the skulls of mice mimicking human Apert syndrome resulting from gain‐of‐function mutation of FGFR2 (P253R)

Apert syndrome is caused mainly by gain‐of‐function mutations of fibroblast growth factor receptor 2. We have generated a mouse model (Fgfr2+/P253R) mimicking human Apert syndrome resulting from fibroblast growth factor receptor 2 Pro253Arg mutation using the knock‐in approach. This mouse model in general has the characteristic skull morphology similar to that in humans with Apert syndrome. To characterize the detailed changes of form in the overall skull and its major anatomic structures, euclidean distance matrix analysis was used to quantitatively compare the form and growth difference between the skulls of mutants and their wild‐type controls. There were substantial morphological differences between the skulls of mutants and their controls at 4 and 8 weeks of age (P