Herring S W, Lakars T C
J Craniofac Genet Dev Biol. 1982;1(4):341-57.
The muscular dysgenesis (mdg) mutation in mice causes developmental arrest of myogenesis at the myotube stage. Stained and cleared skeletal preparations and histological sections of the heads of mdg/mdg and normal mouse fetuses were compared in order to determine the effects of the mutation on craniofacial morphology. Muscles of mastication were more severely affected than tongue muscles. Mutant crania had more domed vaults and slender zygomatic arches that were displaced dorsally. The posterior part of the dysgenic mandible was bent dorsally and compressed dorsoventrally. These shape changes may be the distorting effects of persistent cervical kyphosis. Measurements of camera lucida tracings indicated that the lengths of the total mandible, the angular cartilage and process, and the condylar cartilage and process were similar between mutant and control mice. However, the widths of the condylar and angular cartilages were greatly decreased in the mutants. Moreover, the cartilages of dysgenic mice showed no size increase between 18 and 20 days of gestation. The diminished cartilages presumably result from the absence of mechanical loading from prenatal muscle function. For both condylar and angular cartilages, normal muscle activity should produce compression along the long axis of the cartilage and bending/shearing perpendicular to the long axis. It is argued that these forces are more important in promoting growth in cartilage width than length, accounting for the selective reduction of widths in the dysgenic mutant.