Related Experiment Video
Updated: May 2, 2026

07:13
Measuring Active and Passive Tameness Separately in Mice
Published on: August 10, 2018
6.6K
Differential gene expression in high- and low-active inbred mice
Michelle Dawes1, Trudy Moore-Harrison2, Alicia T Hamilton2
1Department of Health and Kinesiology, Texas A&M University, College Station, TX 77843, USA ; Sydney and JL Huffines Institute for Sports Medicine and Human Performance, Texas A&M University, College Station, TX 77843, USA.
Biomed Research International
|February 20, 2014
Summary
Genetic variations and gene expression in mice do not fully explain differences in physical activity levels. Further research is needed to understand the complex genetic regulation of voluntary exercise behavior.
Area of Science:
- Genetics
- Exercise Physiology
- Molecular Biology
Background:
- Candidate genes for voluntary physical activity regulation are frequently proposed but lack functional validation.
- Understanding the genetic basis of physical activity is crucial for public health and personalized medicine.
Purpose of the Study:
- To investigate the role of candidate genes in regulating physical activity by comparing high- (C57L/J) and low- (C3H/HeJ) active mice.
- To analyze haplotype structure and gene expression profiles of nine candidate genes in skeletal muscle and brain tissues.
Main Methods:
- Gene expression analysis using RT-qPCR for nine candidate genes (Actn2, Actn3, Casq1, Drd2, Lepr, Mc4r, Mstn, Papss2, Slc2a4).
- Single Nucleotide Polymorphism (SNP) analysis in candidate gene regions.
- Comparison of gene expression in skeletal muscle (soleus) and brain between inherently active mouse strains.
Main Results:
- SNPs were identified in Actn2, Casq1, Drd2, Lepr, and Papss2, but not within coding or regulatory sequences.
- Increased Casq1 and Mstn transcript levels in the soleus muscle of low-active mice after running wheel exposure (training effect).
- No significant differential gene expression between high- and low-active mouse strains in naïve animals or significant SNP-based regulatory mechanisms were found.
Conclusions:
- Genomic structural variations and gene expression data alone are insufficient to establish causality for these candidate genes in physical activity regulation.
- The observed differential gene expression was attributed to a training effect, not inherent genetic differences in activity levels.
- Further studies are required to elucidate the complex genetic architecture underlying voluntary physical activity.

