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Msi2-mediated MiR7a-1 processing repression promotes myogenesis.

Wenjun Yang1, Lele Yang2,3, Jianhua Wang4

  • 1Department of Pediatric Orthopedics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University, School of Medicine, Shanghai, China.

Journal of Cachexia, Sarcopenia and Muscle
|December 8, 2021
PubMed
Summary
This summary is machine-generated.

RNA-binding proteins Musashi 2 (Msi2) and human antigen R (HuR) regulate muscle stem cell differentiation by controlling microRNA-7a-1 (MiR7a-1) biogenesis. This pathway is disrupted in aged muscles, impairing regeneration.

Keywords:
HuRMiR7a-1 processingMsi2MyogenesisSkeletal muscle ageing

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Muscle Physiology

Background:

  • MicroRNAs (MiRs) are crucial in myogenesis, but their biogenesis regulation is poorly understood.
  • RNA-binding protein Musashi 2 (Msi2) drives oncogenesis and stem cell proliferation; its role in myogenesis is unexplored.

Purpose of the Study:

  • Investigate Msi2-regulated microRNA biogenesis in myogenesis.
  • Explore the role of Msi2 in muscle stem cell (MuSC) aging and differentiation.

Main Methods:

  • Quantitative RT-PCR, Western blot, and immunoprecipitation identified Msi2 and its binding partner HuR.
  • RNA immunoprecipitation and luciferase assays analyzed Msi2/HuR interaction with MiR7a-1 and its target Cry2.
  • Msi2/HuR knockdown and knockout mouse models assessed in vivo functions.

Main Results:

  • Msi2 and HuR repress MiR7a-1 biogenesis, up-regulating cryptochrome circadian regulator 2 (Cry2) translation.
  • MiR7a-1-mediated down-regulation of Cry2 inhibits MuSC differentiation.
  • Aged muscles show reduced Msi2 and Cry2 levels, correlating with impaired regeneration.

Conclusions:

  • A novel post-transcriptional cascade involving Msi2, HuR, MiR7a-1, and Cry2 regulates myogenesis.
  • Disruption of this cascade in skeletal muscle aging leads to reduced muscle regeneration capacity.