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FTO regulates myoblast proliferation by controlling CCND1 expression in an m6A-YTHDF2-dependent manner

Kaiping Deng1, Zhen Zhang1, Caifang Ren2

  • 1Institute of Sheep and Goat Science, Nanjing Agricultural University, Nanjing, 210095, China.

Experimental Cell Research
|March 2, 2021
PubMed

Insights

Fat mass and obesity-associated (FTO) demethylase is crucial for myoblast proliferation. Knockdown of FTO inhibits myoblast proliferation and promotes apoptosis by decreasing cyclin D1 expression.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Epigenetics

Background:

  • N6-Methyladenosine (m6A) is the most prevalent mRNA modification, regulating key biological processes.
  • The role of the m6A demethylase fat mass and obesity-associated (FTO) in myoblast proliferation remains largely unexplored.

Purpose of the Study:

  • To investigate the function of FTO in myoblast proliferation and its underlying molecular mechanisms.

Main Methods:

  • FTO knockdown was performed in myoblasts.
  • Cell proliferation and apoptosis were assessed.
  • RNA sequencing was utilized to identify differentially expressed genes.
  • Cyclin D1 (CCND1) expression and its regulation were analyzed.

Main Results:

  • FTO knockdown significantly inhibited myoblast proliferation and induced apoptosis.
  • RNA sequencing revealed downregulation of cell cycle and apoptosis-related genes upon FTO silencing.
  • FTO depletion led to decreased CCND1 expression via YTHDF2-mediated mRNA degradation, causing G1 phase delay.
  • Myoblast proliferation was impaired due to reduced CCND1 levels.

Conclusions:

  • FTO plays a critical role in regulating myoblast proliferation.
  • FTO controls CCND1 expression in an m6A-YTHDF2-dependent manner.
  • These findings highlight the significance of m6A modification in myoblast proliferation.
Keywords:
Cell cycleCell proliferationFTOMyoblastm(6)A modification

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