Nucleic Acids Research, 2002, Vol. 30, No. 21 4781-4792
© 2002 Oxford University Press
The severe slow growth of 
srs2 rqh1 in Schizosaccharomyces pombe is suppressed by loss of recombination and checkpoint genes
1 Department of Environmental Health Sciences and 2 Department of Anatomy and Cell Biology, Columbia University, Mailman School of Public Health and College of Physicians and Surgeons, Kolb Building, Room 114, 722 West 168th Street, New York, NY 10032, USA
*To whom correspondence should be addressed. Tel: +1 212 543 4125; Fax: +1 212 781 4993; Email: gaf1{at}columbia.edu
Our interest in the Schizosaccharomyces pombe RecQ helicase, rqh1+, led us to investigate the function of a related putative DNA helicase, srs2+. We identified the srs2+ homolog in S.pombe, and found that srs2+ is not essential for cell viability. A 
srs2 rqh1 double mutant grows extremely slowly with aberrant shaped cells and low viability. This slow growth does not appear to be related to stalled replication, as srs2 rqh1 cells showed higher survival rates, compared with rqh1, when stalled forks were increased by UV irradiation or hydroxy urea treatment. Consistent with this result, we found that srs2 rqh1 cells progress through S-phase with a slight delay, but undergo a checkpoint-dependent arrest presumably at G2/M. Further, we found that srs2 rqh1 slow growth is related to recombination, as loss of either the rhp51+ or rhp57+ recombination genes improves cell growth in the double mutant. srs2 is also synthetic lethal with rhp54, another homologous recombination gene. This lethality is suppressed in a rhp51 background. Together, these results demonstrate a clear genetic interaction between rqh1+, srs2+ and the genes of the homologous recombination pathway.
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