| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print October 17, 2002
Department of Genetic Instability and Cancer, CNRS - IPBS, Toulouse 31077
Corresponding Author: jseb{at}ipbs.fr
We report here that DNA polymerase beta(Pol beta)the base excision repair polymerase, is highly expressed in human melanoma tissues, known to be associated to UV radiation exposure. In order to investigate the potential role of Pol beta in UV-induced genetic instability, we analysed the cellular and molecular effects of excess Pol beta. We firstly demonstrated that mammalian cells overexpressing Pol beta are resistant and hypermutagenic after UV irradiation and that replicative extracts from these cells are able to catalyse complete translesion replication of a thymine–thymine cyclobutane pyrimidine dimer (CPD). By using in vitro primer extension reactions with purified Pol beta, we showed that CPD as well as, at a lesser extent, the 6-4 thymine–thymine pyrimidine–pyrimidone photoproduct (6-4PP) were bypassed. Pol beta mostly incorporates the correct A opposite the 3' T of both CPD and 6-4PP, but can also misinsert C at a frequency of 32% and 26% respectively. In the case of CPD, efficient and error-prone extension of the correct A was found. These data support biological role of Pol beta in UV lesion bypass and suggest that deregulated Pol beta may enhance UV-induced genetic instability.
J. Biol. Chem, 10.1074/jbc.M207101200
Submitted on July 16, 2002
Revised on October 1, 2002
Accepted on October 14, 2002
A role for DNA polymerase beta in mutagenic UV lesions bypass
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  V. K. Batra, D. D. Shock, R. Prasad, W. A. Beard, E. W. Hou, L. C. Pedersen, J. M. Sayer, H. Yagi, S. Kumar, D. M. Jerina, et al. Structure of DNA polymerase beta with a benzo[c]phenanthrene diol epoxide-adducted template exhibits mutagenic features PNAS, November 14, 2006; 103(46): 17231 - 17236. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Donaldson, C. T. Courcelle, and J. Courcelle RuvABC Is Required to Resolve Holliday Junctions That Accumulate following Replication on Damaged Templates in Escherichia coli J. Biol. Chem., September 29, 2006; 281(39): 28811 - 28821. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. V. Gening, S. A. Klincheva, A. Reshetnjak, A. P. Grollman, and H. Miller RNA aptamers selected against DNA polymerase {beta} inhibit the polymerase activities of DNA polymerases beta and kappa. Nucleic Acids Res., January 1, 2006; 34(9): 2579 - 2586. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Boudsocq, P. Benaim, Y. Canitrot, M. Knibiehler, F. Ausseil, J. P. Capp, A. Bieth, C. Long, B. David, I. Shevelev, et al. Modulation of Cellular Response to Cisplatin by a Novel Inhibitor of DNA Polymerase {beta} Mol. Pharmacol., May 1, 2005; 67(5): 1485 - 1492. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Toueille, N. El-Andaloussi, I. Frouin, R. Freire, D. Funk, I. Shevelev, E. Friedrich-Heineken, G. Villani, M. O. Hottiger, and U. Hubscher The human Rad9/Rad1/Hus1 damage sensor clamp interacts with DNA polymerase {beta} and increases its DNA substrate utilisation efficiency: implications for DNA repair Nucleic Acids Res., June 22, 2004; 32(11): 3316 - 3324. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Canitrot, R. Falinski, T. Louat, G. Laurent, C. Cazaux, J.-S. Hoffmann, D. Lautier, and T. Skorski p210 BCR/ABL kinase regulates nucleotide excision repair (NER) and resistance to UV radiation Blood, October 1, 2003; 102(7): 2632 - 2637. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
