QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

doi: 10.1242/10.1242/jcs.00162

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bergoglio, V. Articles by Cazaux, C. Search for Related Content PubMed PubMed Citation Articles by Bergoglio, V. Articles by Cazaux, C.

Localisation of human DNA polymerase to replication foci

Genetic Instability and Cancer, Institut de Pharmacologie et de Biologie Structurale, CNRS UMR 5089, 205 route de Narbonne, 31077 Toulouse Cedex, France

^* Authors for correspondence (e-mail: jseb{at}ipbs.fr; cazaux@ipbs.fr)

Accepted 5 September 2002

The replication of the undamaged genomic DNA requires error-free DNA polymerases and as part of a protein complex that acts continuously along the double helix. In contrast, when the genomic structure is perturbed, DNA replication needs to function more flexibly to bypass DNA distortions. It has been proposed that the newly discovered error prone DNA polymerases play a role in the replication of irregular structure. Here we report that one of them, the human Pol, is mostly localised uniformly in the nucleus of undamaged cells, but could be also concentrated in PCNA-containing replication foci. Following treatment with anti-replicative agents, the proportion of foci-containing cells was increased. These data suggest that Pol may function as part of the replication machinery itself and could be recruited when replicative complexes are stalled. Mutagenesis experiments also indicated that Pol involvement may affect the accuracy of DNA replication. The results are discussed within the context of the oncogenic process since Pol has been found as overexpressed in some cancers.

Key words: Pol, DNA replication, DNA mutagenesis

This article has been cited by other articles:

				C. Guo, T.-S. Tang, M. Bienko, I. Dikic, and E. C. Friedberg Requirements for the Interaction of Mouse Pol{kappa} with Ubiquitin and Its Biological Significance J. Biol. Chem., February 22, 2008; 283(8): 4658 - 4664. [Abstract] [Full Text] [PDF]

				J. L. Youds, N. J. O'Neil, and A. M. Rose Homologous Recombination Is Required for Genome Stability in the Absence of DOG-1 in Caenorhabditis elegans Genetics, June 1, 2006; 173(2): 697 - 708. [Abstract] [Full Text] [PDF]

				J.-Y. Choi and F. P. Guengerich Kinetic Evidence for Inefficient and Error-prone Bypass across Bulky N2-Guanine DNA Adducts by Human DNA Polymerase {iota} J. Biol. Chem., May 5, 2006; 281(18): 12315 - 12324. [Abstract] [Full Text] [PDF]

				X. Bi, L. R. Barkley, D. M. Slater, S. Tateishi, M. Yamaizumi, H. Ohmori, and C. Vaziri Rad18 Regulates DNA Polymerase {kappa} and Is Required for Recovery from S-Phase Checkpoint-Mediated Arrest. Mol. Cell. Biol., May 1, 2006; 26(9): 3527 - 3540. [Abstract] [Full Text] [PDF]

				X. Lin and S. B. Howell DNA mismatch repair and p53 function are major determinants of the rate of development of cisplatin resistance Mol. Cancer Ther., May 1, 2006; 5(5): 1239 - 1247. [Abstract] [Full Text] [PDF]

				J. M. Hinz, R. S. Tebbs, P. F. Wilson, P. B. Nham, E. P. Salazar, H. Nagasawa, S. S. Urbin, J. S. Bedford, and L. H. Thompson Repression of mutagenesis by Rad51D-mediated homologous recombination Nucleic Acids Res., March 6, 2006; 34(5): 1358 - 1368. [Abstract] [Full Text] [PDF]

				Y. Murakumo, S. Mizutani, M. Yamaguchi, M. Ichihara, and M. Takahashi Analyses of ultraviolet-induced focus formation of hREV1 protein Genes Cells, March 1, 2006; 11(3): 193 - 205. [Abstract] [Full Text] [PDF]

				X. Bi, D. M. Slater, H. Ohmori, and C. Vaziri DNA Polymerase {kappa} Is Specifically Required for Recovery from the Benzo[a]pyrene-Dihydrodiol Epoxide (BPDE)-induced S-phase Checkpoint J. Biol. Chem., June 10, 2005; 280(23): 22343 - 22355. [Abstract] [Full Text] [PDF]

				C. Bavoux, A. M. Leopoldino, V. Bergoglio, J. O-Wang, T. Ogi, A. Bieth, J.-G. Judde, S. D. J. Pena, M.-F. Poupon, T. Helleday, et al. Up-Regulation of the Error-Prone DNA Polymerase {kappa} Promotes Pleiotropic Genetic Alterations and Tumorigenesis Cancer Res., January 1, 2005; 65(1): 325 - 330. [Abstract] [Full Text] [PDF]

				T. Ogi, P. Kannouche, and A. R. Lehmann Localisation of human Y-family DNA polymerase {kappa}: relationship to PCNA foci J. Cell Sci., January 1, 2005; 118(1): 129 - 136. [Abstract] [Full Text] [PDF]

				S. Mukhopadhyay, D. R. Clark, N. B. Watson, W. Zacharias, and W. G. McGregor REV1 accumulates in DNA damage-induced nuclear foci in human cells and is implicated in mutagenesis by benzo[a]pyrenediolepoxide Nucleic Acids Res., November 2, 2004; 32(19): 5820 - 5826. [Abstract] [Full Text] [PDF]

				M. Diaz, N. B. Watson, G. Turkington, L. K. Verkoczy, N. R. Klinman, and W. G. McGregor Decreased Frequency and Highly Aberrant Spectrum of Ultraviolet-Induced Mutations in the hprt Gene of Mouse Fibroblasts Expressing Antisense RNA to DNA Polymerase {zeta} Mol. Cancer Res., September 1, 2003; 1(11): 836 - 847. [Abstract] [Full Text] [PDF]