Nutrient Availability Regulates SIRT1 Through a Forkhead-Dependent Pathway

Shino Nemoto, Marı́a M. Fergusson, Toren Finkel

Science · 2004 · 666 citations · 22 references

Concepts

TL;DR

Nutrient availability regulates life‑span across many organisms. Acute nutrient withdrawal in mammalian cells upregulates SIRT1 expression via Foxo3a activation, with Foxo3a binding two p53 sites on the SIRT1 promoter and physically interacting with p53; knockdown of Foxo3a or loss of p53 abolishes this induction, demonstrating that p53, Foxo3a, and SIRT1 form a nutrient‑sensing pathway.

Abstract

Nutrient availability regulates life-span in a wide range of organisms. We demonstrate that in mammalian cells, acute nutrient withdrawal simultaneously augments expression of the SIRT1 deacetylase and activates the Forkhead transcription factor Foxo3a. Knockdown of Foxo3a expression inhibited the starvation-induced increase in SIRT1 expression. Stimulation of SIRT1 transcription by Foxo3a was mediated through two p53 binding sites present in the SIRT1 promoter, and a nutrient-sensitive physical interaction was observed between Foxo3a and p53. SIRT1 expression was not induced in starved p53-deficient mice. Thus, in mammalian cells, p53, Foxo3a, and SIRT1, three proteins separately implicated in aging, constitute a nutrient-sensing pathway.

References

22