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Notch信号通路的调控在出生后肌生成过程中控制卫星细胞的激活和细胞命运决定。

The regulation of Notch signaling controls satellite cell activation and cell fate determination in postnatal myogenesis.

作者信息

Conboy Irina M, Rando Thomas A

机构信息

Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.

出版信息

Dev Cell. 2002 Sep;3(3):397-409. doi: 10.1016/s1534-5807(02)00254-x.

DOI:10.1016/s1534-5807(02)00254-x
PMID:12361602
Abstract

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.

摘要

我们研究了Notch-1及其拮抗剂Numb在出生后肌生成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Pax3的成肌前体细胞的增殖。通过增加Numb表达来减弱Notch信号,导致祖细胞向成肌细胞命运的定向分化以及成肌调节因子、结蛋白和Pax7的表达。在许多中间祖细胞中,Numb在活跃分裂的细胞中不对称定位,这表明存在不对称细胞分裂以及子细胞的不同细胞命运。结果表明,卫星细胞激活导致了关于Notch-1活性的前体细胞异质性群体,并且Notch-1和Numb之间的平衡控制着细胞内稳态和细胞命运决定。

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