A molecular mechanism for direct sirtuin activation by resveratrol

PLoS One. 2012;7(11):e49761. doi: 10.1371/journal.pone.0049761. Epub 2012 Nov 21.

Abstract

Sirtuins are protein deacetylases regulating metabolism, stress responses, and aging processes, and they were suggested to mediate the lifespan extending effect of a low calorie diet. Sirtuin activation by the polyphenol resveratrol can mimic such lifespan extending effects and alleviate metabolic diseases. The mechanism of Sirtuin stimulation is unknown, hindering the development of improved activators. Here we show that resveratrol inhibits human Sirt3 and stimulates Sirt5, in addition to Sirt1, against fluorophore-labeled peptide substrates but also against peptides and proteins lacking the non-physiological fluorophore modification. We further present crystal structures of Sirt3 and Sirt5 in complex with fluorogenic substrate peptide and modulator. The compound acts as a top cover, closing the Sirtuin's polypeptide binding pocket and influencing details of peptide binding by directly interacting with this substrate. Our results provide a mechanism for the direct activation of Sirtuins by small molecules and suggest that activators have to be tailored to a specific Sirtuin/substrate pair.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation / drug effects
  • Caloric Restriction
  • Crystallography, X-Ray
  • Humans
  • Peptides* / chemistry
  • Peptides* / metabolism
  • Protein Binding
  • Protein Conformation
  • Resveratrol
  • Sirtuin 1* / chemistry
  • Sirtuin 1* / metabolism
  • Sirtuin 3* / chemistry
  • Sirtuin 3* / metabolism
  • Sirtuins* / chemistry
  • Sirtuins* / metabolism
  • Stilbenes / pharmacology
  • Substrate Specificity

Substances

  • Peptides
  • Stilbenes
  • SIRT1 protein, human
  • SIRT3 protein, human
  • SIRT5 protein, human
  • Sirtuin 1
  • Sirtuin 3
  • Sirtuins
  • Resveratrol

Grants and funding

This work was supported by FoRUM (grant F539-2007 to C.St.) and Deutsche Forschungsgemeinschaft (STE1701/5 to C. Steegborn, WO1214/3 to D.W.). This publication was funded by the German Research Foundation and the University of Bayreuth in the funding programme Open Access Publishing. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.