JCB logo
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 15 March 2004. doi:10.1083/jcb.200310148
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 164, Number 6, 803-809
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 1453K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gourlay, C. W.
Right arrow Articles by Ayscough, K. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gourlay, C. W.
Right arrow Articles by Ayscough, K. R.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Report

A role for the actin cytoskeleton in cell death and aging in yeast



Campbell W. Gourlay1, Lindsay N. Carpp3, Paul Timpson3, Steven J. Winder2, and Kathryn R. Ayscough1

1 Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield S10 2TN, UK
2 Department of Biomedical Sciences, University of Sheffield, Western Bank, Sheffield S10 2TN, UK
3 Institute of Biomedical and Life Sciences, Division of Biochemistry and Molecular Biology, University of Glasgow, Glasgow G12 8QQ, UK

Address correspondence to Kathryn R. Ayscough, Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield S10 2TN, UK. Tel.: 44 114 222 2332. Fax: 44 114 272 8697. email: k.ayscough{at}sheffield.ac.uk

Several determinants of aging, including metabolic capacity and genetic stability, are recognized in both yeast and humans. However, many aspects of the pathways leading to cell death remain to be elucidated. Here we report a role for the actin cytoskeleton both in cell death and in promoting longevity. We have analyzed yeast strains expressing mutants with either increased or decreased actin dynamics. We show that decreased actin dynamics causes depolarization of the mitochondrial membrane and an increase in reactive oxygen species (ROS) production, resulting in cell death. Important, however, is the demonstration that increasing actin dynamics, either by a specific actin allele or by deletion of a gene encoding the actin-bundling protein Scp1p, can increase lifespan by over 65%. Increased longevity appears to be due to these cells producing lower than wild-type levels of ROS. Homology between Scp1p and mammalian SM22/transgelin, which itself has been isolated in senescence screens, suggests a conserved mechanism linking aging to actin stability.

Key Words: actin; senescence; Scp1; apoptosis; ROS

P. Timpson's present address is The Garvan Institute, Darlinghurst, Sydney, Australia.

Abbreviations used in this paper: ROS, reactive oxygen species; Tpm, tropomyosin.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article

Stay dynamic to slow aging
Karen Birmingham
J. Cell Biol. 2004 164: 793. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents