Nucleic Acids Research Advance Access originally published online on December 14, 2006
Nucleic Acids Research 2007 35(2):353-362; doi:10.1093/nar/gkl1027
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Nucleic Acids Research, 2007, Vol. 35, No. 2 353-362
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Role of Elg1 protein in double strand break repair
1 Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan 2 Tohoku University 21st Century COE Program ‘Comprehensive Research and Education Center for Planning of Drug development and Clinical Evaluation’ Sendai, Miyagi 980-88578, Japan
*To whom correspondence should be addressed. Tel: +81 22 795 6875; Fax: +81 22 795 6873; Email: seki{at}mail.pharm.tohoku.ac.jp
Received September 25, 2006. Revised November 15, 2006. Accepted November 15, 2006.
The inaccurate repair of DNA double-strand breaks (DSBs) can result in genomic instability, and additionally cell death or the development of cancer. Elg1, which forms an alternative RFC-like complex with RFC2-5, is required for the maintenance of genome stability in Saccharomyces cerevisiae, and its function has been linked to DNA replication or damage checkpoint response. Here, we show that Elg1 is involved in homologous recombination (HR)-mediated DSB repair. Mutants of elg1 were partially defective in HR induced by methylmethanesufonate (MMS) and phleomycin. Deletion of ELG1 resulted in less efficient repair of phleomycin-induced DSBs in G2/M phase-arrested cells. During HR between MAT and HML loci, Elg1 associated with both the MAT locus near the HO endonuclease-induced DSB site, and the HML homologous donor locus. The association of Elg1 with the MAT locus was not dependent on Rad52. However, Elg1 association with the HML locus depended on Rad52. Importantly, we found that two of the later steps in HR-mediated repair of an HO endonuclease-induced DSB, primer extension after strand invasion and ligation, were less efficient in elg1 mutants. Our results suggest that Elg1 is involved in DSB repair by HR.
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