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Nucleic Acids Research 2005 33(13):4078-4089; doi:10.1093/nar/gki728
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Published online 21 July 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oupjournals.org

Article

Contrasting effects of Elg1–RFC and Ctf18–RFC inactivation in the absence of fully functional RFC in fission yeast

Jiyoung Kim1, Kathryn Robertson1, Katie J. L. Mylonas1, Fiona C. Gray1,2, Iryna Charapitsa1 and Stuart A. MacNeill1,2,*

1Wellcome Trust Centre for Cell Biology, University of Edinburgh Michael Swann Building, Mayfield Road, Edinburgh EH9 3JR, UK 2Institute of Molecular Biology and Physiology, University of Copenhagen Sølvgade 83H, DK-1307 Copenhagen K, Denmark

*To whom correspondence should be addressed. Tel: +45 35 32 20 05; Fax: +45 35 32 20 40; Email: s.a.macneill{at}mermaid.molbio.ku.dk

Received May 4, 2005. Revised June 16, 2005. Accepted July 5, 2005.

Proliferating cell nuclear antigen loading onto DNA by replication factor C (RFC) is a key step in eukaryotic DNA replication and repair processes. In this study, the C-terminal domain (CTD) of the large subunit of fission yeast RFC is shown to be essential for its function in vivo. Cells carrying a temperature-sensitive mutation in the CTD, rfc1-44, arrest with incompletely replicated chromosomes, are sensitive to DNA damaging agents, are synthetically lethal with other DNA replication mutants, and can be suppressed by mutations in rfc5. To assess the contribution of the RFC-like complexes Elg1–RFC and Ctf18–RFC to the viability of rfc1-44, genes encoding the large subunits of these complexes have been deleted and overexpressed. Inactivation of Ctf18–RFC by the deletion of ctf18+, dcc1+ or ctf8+ is lethal in an rfc1-44 background showing that full Ctf18–RFC function is required in the absence of fully functional RFC. In contrast, rfc1-44 elg1{Delta} cells are viable and overproduction of Elg1 in rfc1-44 is lethal, suggesting that Elg1–RFC plays a negative role when RFC function is inhibited. Consistent with this, the deletion of elg1+ is shown to restore viability to rfc1-44 ctf18{Delta} cells.


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