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Related Experiment Videos

Nutrient availability regulates SIRT1 through a forkhead-dependent pathway.

Shino Nemoto1, Maria M Fergusson, Toren Finkel

  • 1Cardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), Bethesda, MD 20892, USA.

Science (New York, N.Y.)
|December 18, 2004
PubMed
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Nutrient withdrawal activates SIRT1 and Foxo3a in mammalian cells. This pathway, involving p53, Foxo3a, and SIRT1, is crucial for nutrient sensing and may impact aging.

Area of Science:

  • Cellular biology
  • Molecular mechanisms of aging
  • Nutrient sensing pathways

Background:

  • Nutrient availability is a key regulator of lifespan across diverse organisms.
  • SIRT1 deacetylase and Foxo3a transcription factor are implicated in aging processes.

Purpose of the Study:

  • To investigate the interplay between nutrient availability, SIRT1, Foxo3a, and p53 in mammalian cells.
  • To elucidate the molecular mechanisms underlying nutrient sensing.

Main Methods:

  • Acute nutrient withdrawal experiments in mammalian cells.
  • Knockdown of Foxo3a expression.
  • Analysis of SIRT1 promoter activity and p53 binding sites.
  • Co-immunoprecipitation to detect protein-protein interactions.
  • Studies in p53-deficient mice.

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Main Results:

  • Nutrient withdrawal increased SIRT1 expression and activated Foxo3a.
  • Foxo3a knockdown abolished starvation-induced SIRT1 upregulation.
  • Foxo3a directly stimulated SIRT1 transcription via p53 binding sites.
  • A nutrient-sensitive interaction between Foxo3a and p53 was observed.
  • SIRT1 was not induced in starved p53-deficient mice.

Conclusions:

  • Mammalian cells possess a nutrient-sensing pathway involving p53, Foxo3a, and SIRT1.
  • This pathway links nutrient availability to the expression of key aging-related proteins.
  • The findings provide insights into the molecular basis of aging regulation by nutrients.