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Nucleic Acids Research 2005 33(6):1813-1824; doi:10.1093/nar/gki325
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Published online 30 March 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

Dynamic relocalization of hOGG1 during the cell cycle is disrupted in cells harbouring the hOGG1-Cys326 polymorphic variant

Luisa Luna1,2,*, Veslemøy Rolseth1,2, Gunn A. Hildrestrand1,2, Marit Otterlei3, Françoise Dantzer4, Magnar Bjørås2 and Erling Seeberg1,2

1Centre for Molecular Biology and Neuroscience, Institute of Medical Microbiology, University of Oslo Rikshospitalet, N-0027 Oslo, Norway 2Department of Molecular Biology, Institute of Medical Microbiology, University of Oslo Rikshospitalet, N-0027 Oslo, Norway 3Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology N-7489 Trondheim, Norway 4UPR 9003 du Centre National de la Recherche Scientifique, Universite Louis Pasteur, Ecole Superieure de Biotechnologie de Strasbourg 67412 Illkirch Cedex, France

*To whom correspondence should be addressed. Tel: +47 2307 4069; Fax: +47 2307 4061; Email: luisa.luna{at}labmed.uio.no

Received December 7, 2004. Revised March 8, 2005. Accepted March 8, 2005.

Numerous lines of evidence support the role of oxidative stress in different types of cancer. A major DNA lesion, 8-oxo-7,8-dihydroguanine (8-oxoG), is formed by reactive oxygen species in the genome under physiological conditions. 8-OxoG is strongly mutagenic, generating G·C->T·A transversions, a frequent somatic mutation in cancers. hOGG1 was cloned as a gene encoding a DNA glycosylase that specifically recognizes and removes 8-oxoG from 8-oxoG:C base pairs and suppresses G·C->T·A transversions. In this study, we investigated the subcellular localization and expression of hOGG1 during the cell cycle. Northern blots showed cell-cycle-dependent mRNA expression of the two major hOGG1 isoforms. By using a cell line constitutively expressing hOGG1 fused to enhanced green fluorescence protein (EGFP), we observed a dynamic relocalization of EGFP-hOGG1 to the nucleoli during the S-phase of the cell cycle, and this localization was shown to be linked to transcription. A C/G change that results in an amino acid substitution from serine to cysteine in codon 326 has been reported as a genetic polymorphism and a risk allele for a variety of cancers. We investigated the cellular localization of the corresponding protein, hOGG1-Cys326, fused to EGFP and observed a dramatic effect on its localization that is explained by a change in the phosphorylation status of hOGG1.


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