4.7 Article

Spermidine promotes stress resistance in Drosophila melanogaster through autophagy-dependent and -independent pathways

Journal

CELL DEATH & DISEASE
Volume 3, Issue -, Pages -

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/cddis.2012.139

Keywords

Drosophila melanogaster; spermidine; paraquat; oxidative stress; activity; starvation

Categories

Funding

  1. University of St. Andrews
  2. Austrian Science Fund FWF [LIPOTOX, P23490-B12, P24381-B20]
  3. European Commission
  4. Ligue Nationale contre le Cancer (Equipe labellisee)
  5. Agence Nationale pour la Recherche (ANR)
  6. Canceropole Ile-de-France
  7. European Commission (Apo-Sys, ArtForce)
  8. Fondation Axa (Chair for longevity research)
  9. Fondation pour la Recherche Medicale (FRM)
  10. Institut National du Cancer (INCa)
  11. et Fondation Bettencourt-Schueller
  12. Austrian Science Fund (FWF) [P24381] Funding Source: Austrian Science Fund (FWF)
  13. Austrian Science Fund (FWF) [P 24381] Funding Source: researchfish

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The naturally occurring polyamine spermidine (Spd) has recently been shown to promote longevity across species in an autophagy-dependent manner. Here, we demonstrate that Spd improves both survival and locomotor activity of the fruit fly Drosophila melanogaster upon exposure to the superoxide generator and neurotoxic agent paraquat. Although survival to a high paraquat concentration (20mM) was specifically increased in female flies only, locomotor activity and survival could be rescued in both male and female animals when exposed to lower paraquat levels (5 mM). These effects are dependent on the autophagic machinery, as Spd failed to confer resistance to paraquat-induced toxicity and locomotor impairment in flies deleted for the essential autophagic regulator ATG7 (autophagy-related gene 7). Spd treatment did also protect against mild doses of another oxidative stressor, hydrogen peroxide, but in this case in an autophagy-independent manner. Altogether, this study establishes that the protective effects of Spd can be exerted through different pathways that depending on the oxidative stress scenario do or do not involve autophagy. Cell Death and Disease (2012) 3, e401; doi:10.1038/cddis.2012.139; published online 11 October 2012

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