JCB logo
PeproTech: Cell Culture Supplements
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 2 August 2004. doi:10.1083/jcb.200405016
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 166, Number 3, 311-316
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 4282K)
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 Wysocki, R.
Right arrow Articles by Kron, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wysocki, R.
Right arrow Articles by Kron, S. J.
Right arrowPubmed/NCBI databases
*Substance via MeSH
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

Yeast cell death during DNA damage arrest is independent of caspase or reactive oxygen species



Robert Wysocki and Stephen J. Kron

Center for Molecular Oncology and Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, Illinois 60637

Address correspondence to Stephen J. Kron, Center for Molecular Oncology, The University of Chicago, 924 E. 57th Street, Rm. R320, Chicago, IL 60637. Tel.: (773) 834-0250. Fax: (773) 702-4394. email: skron{at}uchicago.edu


Abstract

CDC13 encodes a telomere-binding protein that prevents degradation of telomeres. cdc13-1 yeast grown at the nonpermissive temperature undergo G2/M arrest, progressive chromosome instability, and subsequent cell death. Recently, it has been suggested that cell death in the cdc13-1 mutant is an active process characterized by phenotypic hallmarks of apoptosis and caspase activation. In this work, we show that cell death triggered by cdc13-1 is independent of the yeast metacaspase Yca1p and reactive oxygen species but related to cell cycle arrest per se. Inactivating YCA1 or depleting reactive oxygen species does not increase viability of cdc13-1 cells. In turn, caspase activation does not precede cell death in the cdc13-1 mutant. Yca1p activity assayed by cell binding of mammalian caspase inhibitors is confounded by artifactual labeling of dead yeast cells, which nonspecifically bind fluorochromes. We speculate that during a prolonged cell cycle arrest, cdc13-1 cells reach a critical size and die by cell lysis.

Key Words: FITC-VAD-FMK; apoptosis; CDC13; YCA1; Saccharomyces cerevisiae

Abbreviations used in this paper: DHR123, dihydrorhodamine 123; FMK, fluoromethyl ketone; NAC, N-acetyl-cysteine; PI, propidium iodide; ROS, reactive oxygen species; VAD, valyl-alanyl-aspartyl.


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

Do yeast apoptose?
William A. Wells
J. Cell Biol. 2004 166: 304-305. [Full Text] [PDF]



This article has been cited by other articles:



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