MYOGENIC FACTORS: MUSCLE MATURATION AND REGENERATION

描述（根据研究者摘要逐字附上）：Myf 5和MyoD 在肌肉的规格和/或维持中起关键作用 祖细胞在发育过程中。虽然“敲除”小鼠提供了一个有价值的 用于确定这些因素的哪些功能是独特的， 他们可能重叠，Myf 5基因敲除小鼠出生时死亡限制了 Myf 5缺失肌肉的成熟和再生的研究。通过 将新生的Myf 5缺失的趾长伸肌（EDL）移植到 正常宿主的床（这些肌肉再生并受到神经支配）， 我们可以在Myf 5和MyoD缺失小鼠中比较这些过程。MyoD无效肌 表现出再生缺陷，涉及其卫星细胞的抑制 进行终末分化的能力;然而，这表明Myf 5个无效的成肌细胞发生早熟分化。Myf的比较研究 5 null、MyoD null和野生型肌肉再生将用EM进行 和形态测定分析。Myf 5的缺失对细胞数量的影响 卫星细胞，卫星细胞活化，增殖和终末 将在再生肌肉和体外评估分化。的 缺乏Myf 5对肌肉基因表达的影响（例如，基因编码 MRF、M钙粘蛋白、结蛋白、c-met酪氨酸激酶等）重新激发 肌肉和肌卫星细胞的培养物将用 竞争PCR和免疫组化。将与类似的 正常和MyoD缺失再生肌肉的研究（Sabourin等，1999年）。 Myf 5的缺失对肌肉表型的影响将用 免疫组织化学和凝胶电泳。肌肉疾病的特点是 通过退化再生，再生努力不足， 以跟上退化的步伐。这些研究应该提供线索， 可能会增加肌肉的再生反应。

DESCRIPTION (appended verbatim from investigator's abstract): Myf 5 and MyoD play critical roles in the specification and/or maintenance of muscle progenitor cells during development. While "knock out" mice provide a valuable tool for determining which functions of these factors are unique and the extent to which they might overlap, that Myf 5 null mice die at birth has limited the study of the maturation and regeneration of Myf 5 null muscles. By transplanting newborn Myf 5 null extensor digitorum longus (EDL) muscles into the bed of normal hosts (where these muscle regenerate and become innervated), we can compare these processes in Myf 5 and MyoD null mice. MyoD null muscles exhibits a regeneration deficit involving an inhibition of its satellite cells ability to undergo terminal differentiation; whereas, it is suggested that Myf 5 null myoblasts undergo precocious differentiation. Comparative studies of Myf 5 null, MyoD null and wild type muscle regeneration will be carried out with EM and morphometric analyses. The effect of the absence of Myf 5 on the number of satellite cell, satellite cell activation, proliferation and terminal differentiation will be assessed in regenerating muscle and in vitro. The effects of the absence of Myf 5 on muscle gene expression (e.g., genes encoding the MRFs, M cadhedrin, desmin, c met tyrosine kinase, etc.) in regenerating muscles and in cultures of myosatellite cells will be evaluated with competitive PCR and immunohistochemistry. Comparisons will be made with similar studies of normal and MyoD null regenerating muscle (Sabourin et al., 1999). The effect of the absence of Myf 5 on muscle phenotype will be evaluated with immunohistochemistry and gel electrophoresis. Muscle diseases are characterized by degeneration regeneration, with the regenerative effort being insufficient to keep pace with degeneration. These studies should provide clues to how it may be possible to increase muscle's regenerative response.