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doi:10.1534/genetics.104.037598
A more recent version of this article appeared on June 1, 2005.
REGULAR RESEARCH PAPERS |
A postsynaptic role for Rhp55/57 that is responsible for cell death in 
rqh1 mutants following replication arrest in Schizosaccharomyces pombe
Justin C. Hope 1, Mohamed Maftahi 1 and Greg A Freyer 1*
1 Columbia University
* To whom correspondence should be addressed. E-mail: gaf1{at}columbia.edu.
Submitted on October 14, 2004
Revised on December 14, 2004
Accepted on 2 February 2005
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, which following treatment with hydroxyurea (HU), undergo an aberrant mitosis and 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 function. In addition, this suppression is partially dependent on swi5+. In budding yeast overexpressing Rad51 (the Rhp51 homologue) minimized the need for Rad55/57 (Rhp55/57) in nucleoprotein filament formation. We overexpressed Rhp51 in S. 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 in cells, 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 post synaptic function for Rhp55/57.
Key Words: Rhp55, Rqh1, Swi5, homologous recombination, replication arrest
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