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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
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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.


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