This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lommel, L Articles by Hanawalt, P C Search for Related Content PubMed PubMed Citation Articles by Lommel, L Articles by Hanawalt, P C

 Previous Article  |  Next Article 

Mol Cell Biol. 1993 February; 13(2): 970-976

Increased UV resistance of a xeroderma pigmentosum revertant cell line is correlated with selective repair of the transcribed strand of an expressed gene.

Department of Biological Sciences, Stanford University, California 94305-5020.

ABSTRACT

A UV-resistant revertant (XP129) of a xeroderma pigmentosum group A cell line has been reported to be totally deficient in repair of cyclobutane pyrimidine dimers (CPDs) but proficient in repair of 6-4 photoproducts. This finding has been interpreted to mean that CPDs play no role in cell killing by UV. We have analyzed the fine structure of repair of CPDs in the dihydrofolate reductase gene in the revertant. In this essential, active gene, we observe that repair of the transcribed strand is as efficient as that in normal, repair-proficient human cells, but repair of the nontranscribed strand is not. Within 4 h after UV at 7.5 J/m2, over 50% of the CPDs were removed, and by 8 h, 80% of the CPDs were removed. In contrast, there was essentially no removal from the nontranscribed strand even by 24 h. Our results demonstrate that overall repair measurements can be misleading, and they support the hypothesis that removal of CPDs from the transcribed strands of expressed genes is essential for UV resistance.

This article has been cited by other articles:

• Besaratinia, A., Kim, S.-i., Pfeifer, G. P. (2008). Rapid repair of UVA-induced oxidized purines and persistence of UVB-induced dipyrimidine lesions determine the mutagenicity of sunlight in mouse cells. FASEB J. 22: 2379-2392 [Abstract] [Full Text]  
• Fitch, M. E., Nakajima, S., Yasui, A., Ford, J. M. (2003). In Vivo Recruitment of XPC to UV-induced Cyclobutane Pyrimidine Dimers by the DDB2 Gene Product. J. Biol. Chem. 278: 46906-46910 [Abstract] [Full Text]  
• Geyer, R. K., Nagasawa, H., Little, J. B., Maki, C. G. (2000). Role and Regulation of p53 during an Ultraviolet Radiation-induced G1 Cell Cycle Arrest. Cell Growth Differ. 11: 149-156 [Abstract] [Full Text]  
• Crowley, D. J., Hanawalt, P. C. (1998). Induction of the SOS Response Increases the Efficiency of Global Nucleotide Excision Repair of Cyclobutane Pyrimidine Dimers, but Not 6-4 Photoproducts, in UV-Irradiated Escherichia coli. J. Bacteriol. 180: 3345-3352 [Abstract] [Full Text]  
• Ford, J. M., Hanawalt, P. C. (1997). Expression of Wild-type p53 Is Required for Efficient Global Genomic Nucleotide Excision Repair in UV-irradiated Human Fibroblasts. J. Biol. Chem. 272: 28073-28080 [Abstract] [Full Text]  
• Otrin, V., McLenigan, M, Takao, M, Levine, A., Protic, M (1997). Translocation of a UV-damaged DNA binding protein into a tight association with chromatin after treatment of mammalian cells with UV light. J. Cell Sci. 110: 1159-1168 [Abstract]  
• Donelson, J. E., Donelson, J. E. (1995). Mechanisms of Antigenic Variation in Borrelia hermsii and African Trypanosomes. J. Biol. Chem. 270: 7783-7786 [Full Text]