Institute for Biological and Chemical Systems-Biological Information Processing (IBCS-BIP), Karlsruhe Institute of Technology (KIT), Karlsruhe, Germany.
Leibniz Institute for Age Research (Fritz Lipmann Institute, FLI), Jena, Germany.
Sci Rep. 2021 Jun 18;11(1):12904. doi: 10.1038/s41598-021-92331-8.
The process of myogenesis which operates during skeletal muscle regeneration involves the activation of muscle stem cells, the so-called satellite cells. These then give rise to proliferating progenitors, the myoblasts which subsequently exit the cell cycle and differentiate into committed precursors, the myocytes. Ultimately, the fusion of myocytes leads to myofiber formation. Here we reveal a role for the transcriptional co-regulator nTRIP6, the nuclear isoform of the LIM-domain protein TRIP6, in the temporal control of myogenesis. In an in vitro model of myogenesis, the expression of nTRIP6 is transiently up-regulated at the transition between proliferation and differentiation, whereas that of the cytosolic isoform TRIP6 is not altered. Selectively blocking nTRIP6 function results in accelerated early differentiation followed by deregulated late differentiation and fusion. Thus, the transient increase in nTRIP6 expression appears to prevent premature differentiation. Accordingly, knocking out the Trip6 gene in satellite cells leads to deregulated skeletal muscle regeneration dynamics in the mouse. Thus, dynamic changes in nTRIP6 expression contributes to the temporal control of myogenesis.
在骨骼肌再生过程中进行的成肌发生过程涉及肌肉干细胞的激活,即所谓的卫星细胞。然后,这些细胞产生增殖前体,即成肌细胞,后者随后退出细胞周期并分化为定向前体细胞,即肌细胞。最终,肌细胞的融合导致肌纤维的形成。在这里,我们揭示了转录共调节因子 nTRIP6(LIM 结构域蛋白 TRIP6 的核异构体)在成肌作用的时间控制中的作用。在成肌的体外模型中,nTRIP6 的表达在增殖和分化之间的过渡时短暂地上调,而细胞质异构体 TRIP6 的表达没有改变。选择性阻断 nTRIP6 功能会导致早期分化加速,随后晚期分化和融合失调。因此,nTRIP6 表达的短暂增加似乎可以防止过早分化。相应地,在卫星细胞中敲除 Trip6 基因会导致小鼠骨骼肌再生动力学失调。因此,nTRIP6 表达的动态变化有助于成肌作用的时间控制。