Research Perspective|Volume 3, Issue 12|pp 1163—1168

Sir2 plays a key role in cell fate determination upon SAPK activation

Alexandre Vendrell¹, Francesc Posas

¹Cell Signaling Unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), E-08003, Barcelona, Spain

Received: December 23, 2011Accepted: December 29, 2011Published: December 30, 2011

Copyright: © 2011 Vendrell et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Although the benefit of sirtuin activation in age-related diseases is well-characterized, the benefit of sirtuin activation in acute diseases has been elusive. Here we discuss that, at least in yeast, Sir2 activation prevents programmed cell death induced by the sustained activation of the stress activated protein kinase (SAPK) Hog1, the yeast homologue of the p38 SAPK. Sir2 prevents ROS formation and maximize cell survival upon SAPK activation. The conserved function of Sir2 in age-related diseases and the conserved role of SAPKs open the possibility of a novel role for sirtuins in cell fate determination in eukaryotic cells.