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First published online November 10, 2003

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The Journal of Experimental Biology 206, 4385-4391 (2003)
doi: 10.1242/jeb.00699

Commentary

Controlling muscle mitochondrial content

Christopher D. Moyes

Department of Biology, Queen's University, Kingston, Ontario, Canada, K7L 3N6

(e-mail: moyesc{at}biology.queensu.ca)

Accepted 28 August 2003

Mitochondrial content, a chief determinant of aerobic capacity, varies widely among muscle types and species. Mitochondrial enzyme levels in vertebrate skeletal muscles vary more than 100-fold, from fish white muscle to bird flight muscles. Recent studies have shed light on the transcriptional regulators that control mitochondrial gene expression in muscle fiber differentiation and development, and in the context of pathological conditions such as neuromuscular disease and obesity. While the transcriptional co-activator PGC-1 (peroxisome proliferator-activated receptor gamma co-activator 1) has emerged as a master controller of mitochondrial gene expression, it is important to consider other mechanisms by which coordinated changes in mitochondrial content could arise. These studies, largely using biomedical models, provide important information for comparative biologists interested in the mechanistic basis of inter-species variation in muscle aerobic capacity.

Key words: skeletal muscle, oxidative phosphorylation, energy metabolism, peroxisome proliferator-activated receptor (PPAR), PPAR gamma coactivator 1 (PGC-1)

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