Thayer M J, Tapscott S J, Davis R L, Wright W E, Lassar A B, Weintraub H
Department of Genetics, Hutchinson Cancer Research Center, Seattle, Washington 98104.
Cell. 1989 Jul 28;58(2):241-8. doi: 10.1016/0092-8674(89)90838-6.
Transfection of cDNA expression vectors encoding either MyoD1 or myogenin into 10T1/2 cells converts them to myogenic cells. We show that transfection of 10T1/2 cells with the MyoD1 cDNA activates expression of endogenous MyoD1 mRNA, indicating that MyoD1 is subject to positive autoregulation. This activation of endogenous MyoD1 mRNA was also observed in Swiss 3T6 cells, but not in several other fibroblast or adipoblast cell lines transfected with the MyoD1 cDNA. In addition, transfection of the MyoD1 cDNA leads to activation of myogenin expression, and transfection of the myogenin cDNA leads to activation of MyoD1 expression. Thus, MyoD1 and myogenin appear to function in a positive autoregulatory loop that could either: account for or contribute to the stability of myogenic commitment; or amplify the level of expression of both MyoD1 and myogenin above a critical threshold that is required for activation of the myogenic program.
将编码MyoD1或肌细胞生成素的cDNA表达载体转染到10T1/2细胞中可将它们转化为肌原性细胞。我们发现用MyoD1 cDNA转染10T1/2细胞会激活内源性MyoD1 mRNA的表达,这表明MyoD1受到正向自我调节。在瑞士3T6细胞中也观察到了内源性MyoD1 mRNA的这种激活,但在用MyoD1 cDNA转染的其他几种成纤维细胞或脂肪母细胞系中未观察到。此外,转染MyoD1 cDNA会导致肌细胞生成素表达的激活,而转染肌细胞生成素cDNA会导致MyoD1表达的激活。因此,MyoD1和肌细胞生成素似乎在一个正向自我调节回路中发挥作用,该回路要么:解释或有助于肌原性定向的稳定性;要么将MyoD1和肌细胞生成素的表达水平放大到激活肌原性程序所需的临界阈值以上。