Rudnicki M A, Schnegelsberg P N, Stead R H, Braun T, Arnold H H, Jaenisch R
Institute for Molecular Biology and Biotechnology, McMaster University, Hamilton, Ontario, Canada.
Cell. 1993 Dec 31;75(7):1351-9. doi: 10.1016/0092-8674(93)90621-v.
Mice carrying null mutations in the myogenic regulatory factors Myf-5 or MyoD have apparently normal skeletal muscle. To address whether these two factors functionally substitute for one another in myogenesis, mice carrying mutant Myf-5 and MyoD genes were interbred. While mice lacking both MyoD and Myf-5 were born alive, they were immobile and died soon after birth. Northern blot and S1 nuclease analyses indicated that Myf-5(-1-);MyoD(-1-) mice expressed no detectable skeletal muscle-specific mRNAs. Histological examination of these mice revealed a complete absence of skeletal muscle. Immunohistochemical analysis indicated an absence of desmin-expressing myoblast-like cells. These observations suggest that either Myf-5 or MyoD is required for the determination of skeletal myoblasts, their propagation, or both during embryonic development and indicate that these factors play, at least in part, functionally redundant roles in myogenesis.
在生肌调节因子Myf-5或MyoD中携带无效突变的小鼠具有明显正常的骨骼肌。为了研究这两个因子在肌生成过程中是否在功能上相互替代,将携带突变型Myf-5和MyoD基因的小鼠进行杂交。虽然同时缺乏MyoD和Myf-5的小鼠能够存活出生,但它们无法活动,出生后不久便死亡。Northern印迹和S1核酸酶分析表明,Myf-5(-/-);MyoD(-/-)小鼠未表达可检测到的骨骼肌特异性mRNA。对这些小鼠的组织学检查显示完全没有骨骼肌。免疫组织化学分析表明不存在表达结蛋白的成肌细胞样细胞。这些观察结果表明,在胚胎发育过程中,Myf-5或MyoD对于骨骼肌成肌细胞的确定、增殖或两者都是必需的,并且表明这些因子在肌生成过程中至少部分发挥功能冗余作用。