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miR-16 controls myoblast proliferation and apoptosis through directly suppressing Bcl2 and FOXO1 activities

Xinzheng Jia1, Hongjia Ouyang1, Bahareldin Ali Abdalla1

  • 1Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong 510642, China; Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, and Key Lab of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou, Guangdong 510642, China.

Biochimica Et Biophysica Acta. Gene Regulatory Mechanisms
|March 5, 2017
PubMed

Insights

MicroRNA-16 (miR-16) suppresses avian myogenesis by inhibiting myoblast proliferation and promoting apoptosis. It targets Bcl2 and FOXO1, impacting muscle growth and mass.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Muscle Biology

Background:

  • Myogenesis is a complex process involving myoblast proliferation, differentiation, apoptosis, and fusion.
  • While muscle-specific regulators are known, few microRNAs (miRNAs) have been identified to coordinate these events.
  • Understanding miRNA-mediated regulation is crucial for muscle development and mass maintenance.

Purpose of the Study:

  • To investigate the role of miR-16 in avian myogenesis.
  • To identify the direct molecular targets of miR-16 involved in muscle development.
  • To elucidate the mechanism by which miR-16 regulates myoblast proliferation and apoptosis.

Main Methods:

  • Quantitative analysis of miR-16 expression in chicken pectoral muscle.
  • In vitro experiments to assess the effects of miR-16 on myoblast proliferation and apoptosis.
  • Bioinformatic and biochemical analyses to identify direct targets of miR-16 (Bcl2 and FOXO1).
  • Functional studies involving inhibition of Bcl2 and FOXO1.
  • Chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) to analyze FOXO1-bound genes.

Main Results:

  • miR-16 expression was significantly decreased in hypertrophic pectoral muscle.
  • Overexpression of miR-16 inhibited myoblast proliferation and promoted apoptosis in vitro.
  • Bcl2 and FOXO1 were confirmed as direct targets of miR-16.
  • Inhibition of Bcl2 or FOXO1 mimicked the effects of miR-16 on myogenesis.
  • FOXO1 was identified as a core target mediating growth-related pathways (PI3K-AKT-MAPK, PI3K-AKT-mTOR).
  • ChIP-seq identified 234 FOXO1-bound genes enriched in myogenic proliferation, death, and hypotrophy pathways.

Conclusions:

  • miR-16 acts as a key regulator suppressing avian myogenesis.
  • It controls myoblast proliferation and apoptosis by targeting Bcl2 and FOXO1.
  • FOXO1 plays a central role in mediating miR-16's effects on myogenic pathways.
  • This study reveals a novel mechanism for miR-16 in maintaining skeletal muscle mass.
Keywords:
ApoptosisBcl2FOXO1Myoblast proliferationmiR-16

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