Researchers at Melbourne University, in conjunction with their colleagues at the University of Copenhagen, have published their identification of the C18ORF25 gene in the journal Cell Metabolism.
In their study they tracked the effect of three different types of exercise, resistance, endurance, and sprint, and obtained muscle biopsies after each was completed. They identified almost 6,000 sites that signal activation of proteins and genes (phosophosites) and of these 6,000 they found 420 that were shared between each of the three different forms of exercise.
The researchers identified one of these phosphosites, S67, found on the gene C18ORF25. They then identified C18ORF25 as an AMPK substrate (AMPK being an enzyme that is vital for energy balance within the body and, during exercise, allows the muscles to adapt to the increased energy need) and went further with their study.
In mice they knocked out C18ORF25, thus making it unavailable, and found that when they did this they found that the mice had reduced exercise capacity, muscle fiber size, and contractile function. This indicated that there was also reduced signaling of contractile proteins.
However, when the gene was re-expressed within the mice, these changes reversed and muscle force production returned to normal.
This novel study, which identified the function of C18ORF25, could be the first stepping stone to human therapies that assist in combating a multitude of disorders that effect the skeletal muscle, and even aid in the natural atrophy that occurs as humans age.
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