Abstract
Mitochondrial dysfunction is a hallmark of skeletal muscle degeneration during aging. One mechanism through which mitochondrial dysfunction can be caused is through changes in mitochondrial morphology. To determine the role of mitochondrial morphology changes in age-dependent mitochondrial dysfunction, we studied mitochondrial morphology in body wall muscles of the nematodeC. elegans. We found that in this tissue, animals display a tubular mitochondrial network, which fragments with increasing age. This fragmentation is accompanied by a decrease in mitochondrial volume. Mitochondrial fragmentation and volume loss occur faster under conditions that shorten lifespan and occur slower under conditions that increase lifespan. However, neither mitochondrial morphology nor mitochondrial volume of five- and seven-day old wild-type animals can be used to predict individual lifespan. Our results indicate that while mitochondria in body wall muscles undergo age-dependent fragmentation and a loss in volume, these changes are not the cause of aging but rather a consequence of the aging process.
Highlights
The age-associated degeneration of skeletal muscle function termed ‘sarcopenia’ leads to debilitating conditions among the elderly [1]
With age, www.impactaging.com progressive fragmentation of the mitochondrial network can be observed in body wall muscle cells of C. elegans
Using mitochondrial area as a measure of mitochondrial volume, we found that the volume of mitochondria in muscle cells is significantly reduced in old animals when compared to young animals
Summary
The age-associated degeneration of skeletal muscle function termed ‘sarcopenia’ leads to debilitating conditions among the elderly [1]. Studies in Caenorhabditis elegans, for instance, have revealed that sarcopenia is a feature of aging in nematodes [8]. Due to its short lifespan and its amenability to genetic manipulation, C. elegans is a suitable model to address diverse aspects of sarcopenia [8]. Studies in C. elegans have revealed that lifespan is influenced by gene activity, the environment, certain chemicals as well as stochastic factors [9, 10]. The activation of the C. elegans IGF-1 receptor tyrosine kinase DAF-2 (DAF, dauer larva formation abnormal) induces the activation of the PI3 kinase AGE-1 (AGE, ageing alteration), which leads to the phosphorylation of the FOXO transcription factor DAF-16. Lossof-function mutations in the genes daf-2 or age-1, lead to the nuclear localization of DAF-16 and an increased lifespan, while loss-of-function mutations in daf-16 lead www.impactaging.com
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