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

This Article Full Text Full Text (PDF, 6218K) PPT slides of all figures Supplemental Material Index Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bachant, J. Articles by Fielding, C. S. Search for Related Content PubMed PubMed Citation Articles by Bachant, J. Articles by Fielding, C. S. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB HYDROXYUREA Related Collections Related Article Social Bookmarking                            What's this?

The yeast S phase checkpoint enables replicating chromosomes to bi-orient and restrain spindle extension during S phase distress

Department of Cell Biology and Neuroscience, University of California, Riverside, Riverside, CA 92521

Correspondence to Jeff Bachant: jeffbach{at}citrus.ucr.edu

The budding yeast S phase checkpoint responds to hydroxyurea-induced nucleotide depletion by preventing replication fork collapse and the segregation of unreplicated chromosomes. Although the block to chromosome segregation has been thought to occur by inhibiting anaphase, we show checkpoint-defective rad53 mutants undergo cycles of spindle extension and collapse after hydroxyurea treatment that are distinct from anaphase cells. Furthermore, chromatid cohesion, whose dissolution triggers anaphase, is dispensable for S phase checkpoint arrest. Kinetochore–spindle attachments are required to prevent spindle extension during replication blocks, and chromosomes with two centromeres or an origin of replication juxtaposed to a centromere rescue the rad53 checkpoint defect. These observations suggest that checkpoint signaling is required to generate an inward force involved in maintaining preanaphase spindle integrity during DNA replication distress. We propose that by promoting replication fork integrity under these conditions Rad53 ensures centromere duplication. Replicating chromosomes can then bi-orient in a cohesin-independent manner to restrain untimely spindle extension.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

Related Article

Restraining spindles in distress

Nicole LeBrasseur
J. Cell Biol. 2005 168: 984. [Full Text] [PDF]

This article has been cited by other articles:

• Lu, Y., Cross, F. (2009). Mitotic Exit in the Absence of Separase Activity. Mol. Biol. Cell 20: 1576-1591 [Abstract] [Full Text]  
• Gasparyan, H. J., Xu, L., Petreaca, R. C., Rex, A. E., Small, V. Y., Bhogal, N. S., Julius, J. A., Warsi, T. H., Bachant, J., Aparicio, O. M., Nugent, C. I. (2009). Yeast telomere capping protein Stn1 overrides DNA replication control through the S phase checkpoint. Proc. Natl. Acad. Sci. USA 106: 2206-2211 [Abstract] [Full Text]  
• Warsi, T. H., Navarro, M. S., Bachant, J. (2008). DNA Topoisomerase II Is a Determinant of the Tensile Properties of Yeast Centromeric Chromatin and the Tension Checkpoint. Mol. Biol. Cell 19: 4421-4433 [Abstract] [Full Text]  
• Caldwell, J. M., Chen, Y., Schollaert, K. L., Theis, J. F., Babcock, G. F., Newlon, C. S., Sanchez, Y. (2008). Orchestration of the S-phase and DNA damage checkpoint pathways by replication forks from early origins. JCB 180: 1073-1086 [Abstract] [Full Text]  
• Khalil, A.-M., Julius, J. A., Bachant, J. (2007). One step construction of PCR mutagenized libraries for genetic analysis by recombination cloning. Nucleic Acids Res 0: gkm583v1-12 [Abstract] [Full Text]  
• Ma, L., McQueen, J., Cuschieri, L., Vogel, J., Measday, V. (2007). Spc24 and Stu2 Promote Spindle Integrity When DNA Replication Is Stalled. Mol. Biol. Cell 18: 2805-2816 [Abstract] [Full Text]  
• Woolstencroft, R. N., Beilharz, T. H., Cook, M. A., Preiss, T., Durocher, D., Tyers, M. (2006). Ccr4 contributes to tolerance of replication stress through control of CRT1 mRNA poly(A) tail length. J. Cell Sci. 119: 5178-5192 [Abstract] [Full Text]  
• Roberts, T. M., Kobor, M. S., Bastin-Shanower, S. A., Ii, M., Horte, S. A., Gin, J. W., Emili, A., Rine, J., Brill, S. J., Brown, G. W. (2006). Slx4 Regulates DNA Damage Checkpoint-dependent Phosphorylation of the BRCT Domain Protein Rtt107/Esc4. Mol. Biol. Cell 17: 539-548 [Abstract] [Full Text]  

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