Abstract
We find a dramatic difference in the efficiency of removal of UV-induced pyrimidine dimers from the transcribed and nontranscribed strands of the dihydrofolate reductase (DHFR) gene in cultured hamster and human cells. In hamster cells, 80% of the dimers are removed from the transcribed strand in 4 hr, but little repair occurs in the nontranscribed strand even after 24 hr. In human cells, repair is significantly faster in the transcribed strand than in the other strand. Furthermore, in the 5' flanking region of the human DHFR gene, selective rapid repair occurs in the opposite DNA strand relative to the transcribed strand of the DHFR gene. This strand is thought to serve as a template for transcription of a divergent transcript. These results have important implications for excision repair pathways and mutagenesis in mammalian cells.
| Original language | English |
|---|---|
| Pages (from-to) | 241-249 |
| Number of pages | 9 |
| Journal | Cell |
| Volume | 51 |
| Issue number | 2 |
| DOIs | |
| State | Published - Oct 23 1987 |
Bibliographical note
Funding Information:We thank C. A. Smith and A. K. Ganesan for many helpful discussions and critical readings of the manuscript, E. Wauthier for preparation of T4 endonuclease V, G. Attardi for 6A3 cells and human DHFR plasmids, R. T. Schimke for Bll cells and methotrexate, and L. Chasin for the CHO DHFR plasmid. This work was supported by a grant from the National Cancer Institute (CA35744) and an American Cancer Society Postdoctoral Fellowship (PF-2730) to I. Mellon.
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology