Abstract
Endurance exercise is an inexpensive intervention that is thought to provide substantial protection against several age-related pathologies, as well as inducing acute changes to endurance capacity and metabolism. Recently, it has been established that endurance exercise induces conserved alterations in physiological capacity in the invertebrate Drosophila model. If the genetic factors underlying these exercise-induced physiological alterations are widely conserved, then invertebrate genetic model systems will become a valuable tool for testing of genetic and pharmacological mimetics for endurance training. Here, we assess whether the Drosophila homolog of the vertebrate exercise response gene PGC-1α spargel (srl) is necessary or sufficient to induce exercise-dependent phenotypes. We find that reduction of srl expression levels acutely compromises negative geotaxis ability and reduces exercise-induced improvement in both negative geotaxis and time to exhaustion. Conversely, muscle/heart specific srl overexpression improves negative geotaxis and cardiac performance in unexercised flies. In addition, we find that srl overexpression mimics some, but not all, exercise-induced phenotypes, suggesting that other factors also act in parallel to srl to regulate exercise-induced physiological changes in muscle and heart.
Highlights
In order to facilitate longitudinal studies across ages in model organisms, we have developed an endurance training paradigm in the short lived, genetically tractable Drosophila system
In order to maximize the advantages of an invertebrate genetic model system, it is first important to establish that known genetic components of vertebrate exercise are, conserved in invertebrate models such as Drosophila
The conservation of the molecular role of spargel suggests that its physiological role in response to endurance exercise may be functionally conserved
Summary
In order to facilitate longitudinal studies across ages in model organisms, we have developed an endurance training paradigm in the short lived, genetically tractable Drosophila system. Trained flies exhibit several physiological phenotypes reminiscent of those seen in vertebrate models, including increased motor capacity, cardiac function, and mitochondrial enzyme activity [1]. The most well-studied genetic factor in the vertebrate response to endurance training is the transcriptional co-factor PGC-1a. Chronic training of mammals results in upregulation of PGC-1a transcript [2], while bouts of exercise acutely increase its nuclear localization [3]. Deletion of PGC-1a in mice results in reduced mitochondrial number, blunted postnatal muscle growth, reduced muscle performance and reduced exercise capacity [13]. The extent to which these phenotypes are necessary or sufficient components of broader physiological changes that are induced by endurance exercise is not yet fully understood
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