Reduced expression of frataxin extends the lifespan of Caenorhabditis elegans. Journal Article uri icon



  • 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 nematode Caenorhabditis elegans by 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 in C. elegans.

publication date

  • April 1, 2005

has restriction

  • hybrid

Date in CU Experts

  • September 9, 2013 9:27 AM

Full Author List

  • Ventura N; Rea S; Henderson ST; Condo I; Johnson TE; Testi R

author count

  • 6

citation count

  • 27

Other Profiles

International Standard Serial Number (ISSN)

  • 1474-9718

Electronic International Standard Serial Number (EISSN)

  • 1474-9726

Additional Document Info

start page

  • 109

end page

  • 112


  • 4


  • 2