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J. Biol. Chem., Vol. 277, Issue 41, 38305-38310, October 11, 2002

This Article Full Text Full Text (PDF) All Versions of this Article: 277/41/38305    most recent M206375200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Hu, W. Articles by Tang, M.-s. Search for Related Content PubMed PubMed Citation Articles by Hu, W. Articles by Tang, M.-s. Social Bookmarking                      What's this?

Transcription-coupled and Transcription-independent Repair of Cyclobutane Pyrimidine Dimers in the Dihydrofolate Reductase Gene^*

Wenwei Hu^§, Zhaohui Feng^§, Lawrence A. Chasin^¶, and Moon-shong Tang

From the  Department of Environmental Medicine, Pathology, and Medicine, New York University School of Medicine, Tuxedo, New York 10987 and the ^¶ Department of Biological Sciences, Columbia University, New York, New York 10027

Using a ligation-mediated polymerase chain reaction technique, we have mapped the repair of ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs) at the nucleotide level in exons 1, 2, and 5 of the dihydrofolate reductase (DHFR) gene in Chinese hamster ovary cells. We found that CPDs are preferentially repaired in the transcribed strand (T strand) and that the order of repair efficiency is exon 1 > exon 2 > exon 5. In the cells with a deletion of the DHFR gene encompassing the promoter region and the first four exons, CPDs are not repaired in the T strand of the residual DHFR gene. These results substantiate the idea that the preferential repair of CPDs in the T strand is transcription dependent. However, in the wild type gene we have found that CPDs are efficiently repaired in the nontranscribed strand (NT strand) of exon 1 but not in the NT strand of exons 2 and 5. Probing the chromatin structure of exons 1, 2, and 5 of the DHFR gene with micrococcal nuclease revealed that the exon 1 region is much more sensitive to micrococcal nuclease digestion than the exon 2 and exon 5 regions, suggesting that the chromatin structure in the exon 1 region is much more open. These results suggest that, although preferential repair of the T strand of the DHFR gene is transcription dependent, repair of the NT strand is greatly affected by chromatin structure.

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