MyoD公司
肌发生
生物
骨骼肌
肌动蛋白
肌生成素
肌源性调节因子
皮特x2
心肌细胞
结蛋白
内分泌学
内科学
分子生物学
细胞生物学
肌球蛋白
遗传学
基因
基因表达
免疫学
免疫组织化学
同源盒
波形蛋白
医学
作者
Michael A. Rudnicki,Patrick N.J. Schnegelsberg,R. H. Stead,Thomas Braun,Hans-Henning Arnold,Rudolf Jaenisch
出处
期刊:Cell
[Elsevier]
日期:1993-12-01
卷期号:75 (7): 1351-1359
被引量:1538
标识
DOI:10.1016/0092-8674(93)90621-v
摘要
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.
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