Molecular Biology of the Cell Call for Nominations: MBC Editor-in-Chief

Home Help [Feedback] [For Subscribers] [Archive] [Search] --
QUICK SEARCH:   [advanced]


     

MBC in Press, published online ahead of print November 10, 2004
Mol. Biol. Cell 10.1091/mbc.E04-09-0833

A more recent version of this article appeared on January 1, 2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
E04-09-0833v1
16/1/421    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Green, B.
Right arrow Articles by Li, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Green, B.
Right arrow Articles by Li, J.

Submitted on September 23, 2004
Revised on October 26, 2004
Accepted on October 28, 2004

Loss of Rereplication Control in Saccharomyces cerevisiae Results in Extensive DNA Damage

Brian Green* and Joachim Li{dagger}{ddagger}

Departments of *Biochemistry and Biophysics and {dagger}Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143-2200

Monitoring Editor: Orna Cohen-Fix

To maintain genome stability, the entire genome of a eukaryotic cell must be replicated once and only once per cell cycle. In many organisms, multiple overlapping mechanisms block rereplication, but the consequences of deregulating these mechanisms are poorly understood. Here we show that disrupting these controls in the budding yeast S. cerevisiae rapidly blocks cell proliferation. Rereplicating cells activate the classical DNA damage-induced checkpoint response, which depends on the BRCT checkpoint protein Rad9. In contrast, Mrc1, a checkpoint protein required for recognition of replication stress, does not play a role in the response to rereplication. Strikingly, rereplicating cells accumulate subchromosomal DNA breakage products. These rapid and severe consequences suggest that even limited and sporadic rereplication could threaten the genome with significant damage. Hence, even subtle disruptions in the cell cycle regulation of DNA replication may predispose cells to the genomic instability associated with tumorigenesis.

{ddagger}Corresponding author. E-mail: jli{at}itsa.ucsf.edu






Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Copyright © 2004 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.