- THIS ARTICLE
- Full Text
- Full Text (PDF)
-
All Versions of this Article:
genetics.104.037598v1
170/2/519 most recent - Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Hope, J. C.
- Articles by Freyer, G. A.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Hope, J. C.
- Articles by Freyer, G. A.
Originally published as Genetics Published Articles Ahead of Print on March 31, 2005.
Genetics, Vol. 170, 519-531, June 2005, Copyright © 2005
doi:10.1534/genetics.104.037598
A Postsynaptic Role for Rhp55/57 That Is Responsible for Cell Death in 
rqh1 Mutants Following Replication Arrest in Schizosaccharomyces pombe
Justin C. Hope*,
Mohamed Maftahi
and
Greg A. Freyer*,,1
* Graduate Program in Anatomy and Cell Biology, Department of Anatomy and Cell Biology
Department of Environmental Health Sciences, Mailman School of Public Health and College of Physicians and Surgeons, Columbia University, New York, New York 10032
1 Corresponding author: Kolb Bldg., Room 140, Columbia University, 722 W. 168th St., New York, NY 10032.
E-mail: gaf1{at}columbia.edu
Following replication arrest, multiple cellular responses are triggered to maintain genomic integrity. In fission yeast, the RecQ helicase, Rqh1, plays a critical role in this process. This is demonstrated in 
rqh1 cells that, following treatment with hydroxyurea (HU), undergo an aberrant mitosis leading to cell death. Previous data suggest that Rqh1 functions with homologous recombination (HR) in recovery from replication arrest. We have found that loss of the HR genes rhp55+ or rhp57+, but not rhp51+ or rhp54+, suppresses the HU sensitivity of rqh1 cells. Much of this suppression requires Rhp51 and Rhp54. In addition, this suppression is partially dependent on swi5+. In budding yeast, overexpressing Rad51 (the Rhp51 homolog) minimized the need for Rad55/57 (Rhp55/57) in nucleoprotein filament formation. We overexpressed Rhp51 in Schizosaccharomyces pombe and found that it greatly reduced the requirement for Rhp55/57 in recovery from DNA damage. However, overexpressing Rhp51 did not change the rhp55 suppression of the HU sensitivity of rqh1, supporting an Rhp55/57 function during HR independent of nucleoprotein filament formation. These results are consistent with Rqh1 playing a role late in HR following replication arrest and provide evidence for a postsynaptic function for Rhp55/57.
This article has been cited by other articles:
 |
|
 |
|
  J. C. Hope, L. D. Cruzata, A. Duvshani, J. Mitsumoto, M. Maftahi, and G. A. Freyer Mus81-Eme1-Dependent and -Independent Crossovers Form in Mitotic Cells during Double-Strand Break Repair in Schizosaccharomyces pombe Mol. Cell. Biol., May 15, 2007; 27(10): 3828 - 3838. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Ampatzidou, A. Irmisch, M. J. O'Connell, and J. M. Murray Smc5/6 Is Required for Repair at Collapsed Replication Forks Mol. Cell. Biol., December 15, 2006; 26(24): 9387 - 9401. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. C. Hope, S. M. Mense, M. Jalakas, J. Mitsumoto, and G. A. Freyer Rqh1 blocks recombination between sister chromatids during double strand break repair, independent of its helicase activity PNAS, April 11, 2006; 103(15): 5875 - 5880. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Pebernard, J. Wohlschlegel, W. H. McDonald, J. R. Yates III, and M. N. Boddy The nse5-nse6 dimer mediates DNA repair roles of the smc5-smc6 complex. Mol. Cell. Biol., March 1, 2006; 26(5): 1617 - 1630. [Abstract] [Full Text] [PDF]
|
|