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MBC in Press, published online ahead of print August 1, 2007
Mol. Biol. Cell 10.1091/mbc.E07-05-0490

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Submitted on May 24, 2007
Revised on July 18, 2007
Accepted on July 20, 2007

Shu Proteins Promote the Formation of Homologous Recombination Intermediates that Are Processed by Sgs1-Rmi1-Top3

Hocine W. Mankouri, Hien-Ping Ngo, and Ian D. Hickson

Cancer Research UK Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DS, United Kingdom

Monitoring Editor: Wendy Bickmore

CSM2, PSY3, SHU1 and SHU2 (collectively referred to as the SHU genes) were identified in S. cerevisiae as four genes in the same epistasis group that suppress various sgs1 and top3 mutant phenotypes when mutated. Although the SHU genes have been implicated in homologous recombination repair (HRR), their precise role(s) within this pathway remains poorly understood. Here, we have identified a specific role for the Shu proteins in a Rad51/Rad54-dependent HRR pathway(s) to repair MMS-induced lesions during S-phase. We show that, whereas mutation of RAD51 or RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising during replication in sgs1 cells, mutation of SHU genes attenuated the level of these structures. Similar findings were also observed in shu1 cells in which Rmi1 or Top3 function was impaired. We propose a model in which the Shu proteins act in HRR to promote the formation of HRR intermediates that are processed by the Sgs1-Rmi1-Top3 complex.

Address correspondence to: Ian D. Hickson (ian.hickson{at}cancer.org.uk)




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E. Coic, T. Feldman, A. S. Landman, and J. E. Haber
Mechanisms of Rad52-Independent Spontaneous and UV-Induced Mitotic Recombination in Saccharomyces cerevisiae
Genetics, May 1, 2008; 179(1): 199 - 211.
[Abstract] [Full Text] [PDF]


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