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O-GlcNAc transferase is required to maintain satellite cell function.

Morgan D Zumbaugh1, Ashley E Geiger1, Jing Luo1

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Stem Cells (Dayton, Ohio)
|February 26, 2021
PubMed
Summary

O-GlcNAcylation, regulated by O-GlcNAc transferase (OGT), is vital for muscle satellite cell (SC) health. Loss of OGT impairs SC function, proliferation, and self-renewal, impacting muscle repair.

Keywords:
UDP-O-GlcNAcmuscle stem cellsnutrient sensingregenerative myogenesis

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Muscle Physiology

Background:

  • O-GlcNAcylation acts as a nutrient sensor in various cells.
  • The role of O-GlcNAcylation in muscle satellite cells (SCs) is not well understood.

Purpose of the Study:

  • To investigate the function of O-GlcNAcylation in muscle satellite cells.
  • To determine the impact of O-GlcNAc transferase (OGT) deficiency on SCs in muscle repair.

Main Methods:

  • Genetic ablation of OGT in mouse SCs.
  • In vivo muscle injury model and SC function evaluation.
  • Doxycycline-inducible H2B-GFP mouse model for tracing SC cycling.
  • In vitro, ex vivo, and in vivo proliferation assays.

Main Results:

  • OGT-deficient SCs showed impaired muscle repair capacity after injury.
  • SCs lacking OGT exhibited reduced cycling rates and abundance over time.
  • Self-renewal and proliferation capabilities of OGT-deficient SCs were significantly decreased.
  • Cell cycle arrest, potentially HCF1-mediated, was observed in OGT-deficient SCs.

Conclusions:

  • O-GlcNAcylation is essential for maintaining muscle satellite cell health and function.
  • OGT plays a critical role in SC response to normal and injured skeletal muscle conditions.
  • O-GlcNAcylation is crucial for SC proliferation and self-renewal, impacting muscle regeneration.