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- Title
Reduced expression of frataxin extends the lifespan ofCaenorhabditis elegans.
- Authors
Ventura, Natascia; Rea, Shane; Henderson, Samuel T.; Condo, Ivano; Johnson, Thomas E.; Testi, Roberto
- Abstract
Defects in the expression of the mitochondrial protein frataxin cause Friedreich's ataxia, an hereditary neurodegenerative syndrome characterized by progressive ataxia and associated with reduced life expectancy in humans. Homozygous inactivation of the frataxin gene results in embryonic lethality in mice, suggesting that frataxin is required for organismic survival. Intriguingly, the inactivation of many mitochondrial genes in the nematodeCaenorhabditis elegansby RNAi extends lifespan. We therefore investigated whether inactivation of frataxin by RNAi-mediated suppression of the frataxin homolog gene (frh-1) would also prolong lifespan in the nematode. Frataxin-deficient animals have a small body size, reduced fertility and altered responses to oxidative stress. Importantly, frataxin suppression by RNAi significantly extends lifespan inC. elegans.
- Subjects
AGING; DEVELOPMENTAL biology; FRIEDREICH'S ataxia; CEREBELLUM degeneration; MITOCHONDRIA
- Publication
Aging Cell, 2005, Vol 4, Issue 2, p109
- ISSN
1474-9718
- Publication type
Other
- DOI
10.1111/j.1474-9726.2005.00149.x