Reduced expression of frataxin extends the lifespan of Caenorhabditis elegans

Natascia Ventura, Shane Rea, Samuel T. Henderson, Ivano Condo, Thomas E. Johnson, Roberto Testi

Research output: Contribution to journalArticlepeer-review

62 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)109-112
Number of pages4
JournalAging cell
Issue number2
StatePublished - Apr 2005
Externally publishedYes


  • Aging
  • Frataxin
  • Friedreich's Ataxia
  • Mitochondria

ASJC Scopus subject areas

  • Aging
  • Cell Biology


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