The increases in the skeletal muscle mass of the transgenic mice expressing the mutated myostatin affected craniofacial morphology

Myostatin, which is a member of the TGF-β superfamily, is a negative regulator of skeletal muscle formation. Myostatin null mice showed a doubling of their muscle mass compared to normal mice. In a previous study, we generated transgenic mice expressing the mutated myostatin containing an 11-nucleotide deletion that caused a frame-shift mutation. We identified that the transgenic mice exhibited dramatic increases in the skeletal muscle mass resulting from hyperplasia without hypertrophy. In this study, we examined the craniofacial morphology of the transgenic mice to assess the effects of the increased muscle mass on the skeletal growth and development. The craniums and mandibles of age-matched adult mutant mice and their normal littermates were compared. The byzigomatic width of the transgenic mice was larger than that of the control littermates. The mandible of the transgenic mice had increased in size. The coronoid process and angular process of the transgenic mice had developed particularly longer than those of the control littermates. The masseteric ridge of the transgenic mice, in which the deep masseter muscle was inserted, developed more than that of the control littermates. These results show that the increased muscle mass affected the regions of the cranium and mandible where the jaw muscles are specifically attached.