The regulation of notch signaling controls satellite cell activation and cell fate determination in postnatal myogenesis
The regulation of notch signaling controls satellite cell activation and cell fate determination in postnatal myogenesis
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DOI：
10.1016/s1534-5807(02)00254-x
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发表时间：
2002-09-01
影响因子：
11.8
通讯作者：
Rando, TA
中科院分区：
文献类型：
--
作者：
Conboy, IM;Rando, TA
我们研究了Notch-1及其拮抗剂Numb在出生后肌发生过程中卫星细胞激活中的作用。Notch-1的激活促进了表达前成肌细胞标志物Pax 3的肌源性前体细胞的增殖。通过增加Numb表达减弱Notch信号传导导致祖细胞向成肌细胞命运的承诺以及肌源性调节因子、结蛋白和Pax 7的表达。在许多中间祖细胞中，Numb不对称地定位于活跃分裂的细胞中，表明子细胞的不对称细胞分裂和不同的细胞命运。结果表明，卫星细胞活化导致在Notch-1活性方面的前体细胞的异质群体，并且Notch-1和Numb之间的平衡控制细胞稳态和细胞命运决定。
We have studied the role of Notch-1 and its antagonist Numb in the activation of satellite cells during postnatal myogenesis. Activation of Notch-1 promoted the proliferation of myogenic precursor cells expressing the premyoblast marker Pax3. Attenuation of Notch signaling by increases in Numb expression led to the commitment of progenitor cells to the myoblast cell fate and the expression of myogenic regulatory factors, desmin, and Pax7. In many intermediate progenitor cells, Numb was localized asymmetrically in actively dividing cells, suggesting an asymmetric cell division and divergent cell fates of daughter cells. The results indicate that satellite cell activation results in a heterogeneous population of precursor cells with respect to Notch-1 activity and that the balance between Notch-1 and Numb controls cellular homeostasis and cell fate determination.