JCB logo
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 27 November 2006. doi:10.1083/jcb.200605080
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 175, Number 5, 729-741
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 4101K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
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 Enserink, J. M.
Right arrow Articles by Kolodner, R. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Enserink, J. M.
Right arrow Articles by Kolodner, R. D.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene
*Substance via MeSH
Related Collections
Right arrowRelated Articles
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Article

Checkpoint proteins control morphogenetic events during DNA replication stress in Saccharomyces cerevisiae



Jorrit M. Enserink1, Marcus B. Smolka1, Huilin Zhou1,3,4, and Richard D. Kolodner1,2,3,4

1 Ludwig Institute for Cancer Research, 2 Department of Medicine, 3 Department of Cellular and Molecular Medicine, and 4 Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA 92093

Correspondence to Richard D. Kolodner: rkolodner{at}ucsd.edu

In response to DNA replication stress in Saccharomyces cerevisiae, the DNA replication checkpoint maintains replication fork stability, prevents precocious chromosome segregation, and causes cells to arrest as large-budded cells. The checkpoint kinases Mec1 and Rad53 act in this checkpoint. Treatment of mec1 or rad53{Delta} mutants with replication inhibitors results in replication fork collapse and inappropriate partitioning of partially replicated chromosomes, leading to cell death. We describe a previously unappreciated function of various replication stress checkpoint proteins, including Rad53, in the control of cell morphology. Checkpoint mutants have aberrant cell morphology and cell walls, and show defective bud site selection. Rad53 shows genetic interactions with septin ring pathway components, and, along with other checkpoint proteins, controls the timely degradation of Swe1 during replication stress, thereby facilitating proper bud growth. Thus, checkpoint proteins play an important role in coordinating morphogenetic events with DNA replication during replication stress.

Abbreviations used in this paper: CDK, cyclin-dependent kinase; HU, hydroxyurea; YPD, yeast extract/peptone/dextrose.


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 Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?

Related Articles

Damage stops bud growth
Nicole LeBrasseur
J. Cell Biol. 2006 175: 677b. [Full Text] [PDF]

An FHA domain–mediated protein interaction network of Rad53 reveals its role in polarized cell growth
Marcus B. Smolka, Sheng-hong Chen, Paul S. Maddox, Jorrit M. Enserink, Claudio P. Albuquerque, Xiao X. Wei, Arshad Desai, Richard D. Kolodner, and Huilin Zhou
J. Cell Biol. 2006 175: 743-753. [Abstract] [Full Text] [PDF]



This article has been cited by other articles:



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