Congenic strains confirm aerobic running capacity quantitative trait loci on rat chromosome 16 and identify possible intermediate phenotypes

Author:

Ways Justin A.1,Smith Brian M.2,Barbato John C.3,Ramdath Ramona S.1,Pettee Krista M.1,DeRaedt Sarah J.1,Allison David C.2,Koch Lauren G.4,Lee Soon Jin1,Cicila George T.1

Affiliation:

1. Departments of Physiology, Pharmacology, Metabolism, and Cardiovascular Sciences, University of Toledo College of Medicine, Toledo

2. Department of Surgery, University of Toledo College of Medicine, Toledo

3. Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio

4. Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, Michigan

Abstract

We previously identified two inbred rat strains divergent for treadmill aerobic running capacity (ARC), the low-performing Copenhagen (COP) and the high-performing DA rats, and used an F2(COP×DA) population to identify ARC quantitative trait loci (QTLs) on rat chromosome 16 (RNO16) and the proximal portion of rat chromosome 3 (RNO3). Two congenic rat strains were bred to further investigate these ARC QTLs by introgressing RNO16 and the proximal portion of RNO3 from DA rats into the genetic background of COP rats and were named COP.DA(chr 16) and COP.DA(chr 3), respectively. COP.DA(chr 16) rats had significantly greater ARC compared with COP rats (696.7 ± 38.2 m vs. 571.9 ± 27.5 m, P = 0.03). COP.DA(chr 3) rats had increased, although not significant, ARC compared with COP rats (643.6 ± 40.9 m vs. 571.9 ± 27.5 m). COP.DA(chr 16) rats had significantly greater subcutaneous abdominal fat, as well as decreased fasting triglyceride levels, compared with COP rats ( P < 0.05), indicating that genes responsible for strain differences in fat metabolism are also located on RNO16. While this colocalization of QTLs may be coincidental, it is also possible that these differences in energy balance may be associated with the superior running performance of COP.DA(chr 16) consomic rats.

Publisher

American Physiological Society

Subject

Genetics,Physiology

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