Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow Print PDF (219K) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (10)
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Germanier, M.
Right arrow Articles by Larminat, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Germanier, M.
Right arrow Articles by Larminat, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2000, Vol. 28, No. 23 4674-4678
© 2000 Oxford University Press

Transcription-coupled repair is inducible in hamster cells

Maryse Germanier, Martine Defais, Vilhelm A. Bohr1 and Florence Larminat*

Institut de Pharmacologie et de Biologie Structurale, UMR 5089, CNRS, 205 Route de Narbonne, 31400 Toulouse, France and 1Laboratory of Molecular Genetics, NIA, NIH, Baltimore, MD, USA

In mammalian cells, the rate of nucleotide excision repair of UV dimers is heterogeneous throughout the genome, with repair occurring more rapidly in the transcribed strand of active genes than in the genome overall. This repair pathway is termed transcription-coupled repair (TCR) and is thought to permit the rapid resumption of RNA synthesis following UV irradiation. To evaluate the inducibility of the TCR process, we examined the repair of UV-induced cyclobutane pyrimidine dimers (CPDs) at the level of the gene following exposure of hamster cells to a sub-lethal UV fluence, 3 h prior to a higher dose. Repair was detected by a well-established technique allowing quantification of CPDs at the level of a specific strand by Southern blot hybridization. Here, we show that prior low-dose irradiation clearly enhanced the early rate of CPD removal in the transcribed strand of the active DHFR gene. Furthermore, the RNA synthesis recovery following UV exposure was stimulated by the priming UV dose. Thus, we provide evidence for an inducible TCR response to CPDs in hamster cells. This pathway is independent of the p53 activation, since the hamster cell line that we used expresses high levels of mutant p53 protein.

* To whom correspondence should be addressed. Tel: +33 5 61175986; Fax: +33 5 61175994; Email: flol{at}ipbs.fr


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cancer Res.Home page
L. L. Bedard, M. Alessi, S. Davey, and T. E. Massey
Susceptibility to Aflatoxin B1-Induced Carcinogenesis Correlates with Tissue-Specific Differences in DNA Repair Activity in Mouse and in Rat
Cancer Res., February 15, 2005; 65(4): 1265 - 1270.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.