Missing gene turns mice into distance runners

The total number of nuclei in EDL muscles from B6129 and IL-15RaKO mice

How are endurance athletes able to perform at such high-levels in sport? Most would attribute this athleticism to dedication and countless hours of training. However, a group of researchers headed by Dr. Tejvir Khurana at the University of Pennsylvania suggest that muscle endurance may be linked to a gene called IL-15Rα that is either missing or contains single nucleotide polymorphisms (i.e., a gene mutation) in muscle tissue. They found that mice deficient in the IL-15Rα gene had greater endurance capacity and fatigue resistance than their wildtype counterparts. Perhaps one day drugs will be designed to silence IL-15Rα so that we can all run like Olympic-class endurance athletes.

From the source article by Sarah C.P. Williams :
Previous studies had suggested that IL-15Rα is important for muscle strength. In experiments on cells grown in a Petri dish, the gene seemed to control the accumulation of proteins necessary for muscle contraction. But IL-15Rα had never been studied in a living animal.

In the new research, physiologist Tejvir Khurana of the University of Pennsylvania and his colleagues genetically engineered mice to lack the IL-15Rα gene. The changes were dramatic. Each night, according to sensors on the wheels in the mice's cages, the modified mice ran six times farther than normal mice.

But these behavioral quirks weren't quite enough to convince Khurana of the effect on muscles. Lack of the IL-15Rα gene could just be making the mice jittery or giving them extra energy. So the researchers dissected muscles from the longer-running mice. The muscles sported increased numbers of energy-generating mitochondria and more muscle fibers, indicating that they tired less easily. And when the researchers stimulated them with electricity, the muscles continued to contract for longer than normal, taking longer to use up their energy stores, the team reports in The Journal of Clinical Investigation.

Source
Original research article

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