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BioMed Research International
Volume 2014 (2014), Article ID 361048, 9 pages
Research Article

Differential Gene Expression in High- and Low-Active Inbred Mice

1Department of Health and Kinesiology, Texas A&M University, College Station, TX 77843, USA
2Sydney and JL Huffines Institute for Sports Medicine and Human Performance, Texas A&M University, College Station, TX 77843, USA
3Department of Kinesiology, University of North Carolina Charlotte, Charlotte, NC 28223, USA
4Department of Animal Science, Texas A&M University, College Station, TX 77843, USA

Received 15 October 2013; Accepted 15 December 2013; Published 16 January 2014

Academic Editor: Jaakko Kaprio

Copyright © 2014 Michelle Dawes et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Numerous candidate genes have been suggested in the recent literature with proposed roles in regulation of voluntary physical activity, with little evidence of these genes’ functional roles. This study compared the haplotype structure and expression profile in skeletal muscle and brain of inherently high- (C57L/J) and low- (C3H/HeJ) active mice. Expression of nine candidate genes [Actn2, Actn3, Casq1, Drd2, Lepr, Mc4r, Mstn, Papss2, and Glut4 (a.k.a. Slc2a4)] was evaluated via RT-qPCR. SNPs were observed in regions of Actn2, Casq1, Drd2, Lepr, and Papss2; however, no SNPs were located in coding sequences or associated with any known regulatory sequences. In mice exposed to a running wheel, Casq1 ( ) and Mstn ( ) transcript levels in the soleus were higher in the low-active mice. However, when these genes were evaluated in naïve animals, differential expression was not observed, demonstrating a training effect. Among naïve mice, no genes in either tissue exhibited differential expression between strains. Considering that no obvious SNP mechanisms were determined or differential expression was observed, our results indicate that genomic structural variation or gene expression data alone is not adequate to establish any of these genes’ candidacy or causality in relation to regulation of physical activity.