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Nucleic Acids Research, 1988, Vol. 16, No. 15 7397-7403
© 1988

Articles

Human repair gene restores normal pattern of preferential DNA repair in repair defective CHO cells

Vilhelm A. Bohr, Ernest H.Y. Chu1, Marcel van Duin2, Philip C. Hanawalt+ and Diane S. Okumoto

Laboratory of Molecular Pharmacology Bldg 37, Rm 5-A19 National Cancer Institute, NIH Bethesda, MD 20892, USA 1Department of Human Genetics, University of Michigan Medical School Ann Arbor, MI 48109, USA 2Department of Cell Biology and Genetics, Erasmus University PO Box 1738, 3000 DR, Rotterdam, The Netherlands +Department of Biological Sciences, Stanford University Stanford, CA 94305-5020, USA

Received May 13, 1988. Revised July 7, 1988. Accepted July 7, 1988.

The pattern of preferential DNA repair of UV-induced pyr1n1d1ne dimers was studied in repair-deficient Chinese hamster ovary (CHO) cells transfected with the human excision repair gene, ERCC-1. Repair efficiency was measured 1n the active dihydrofolate reductase (DHFR) gene and 1n Its flanking, non-transcribed sequences in three cell lines: Wild type CHO cells, a UV-sensitive excision deficient CHO mutant, and the transfected line of the mutant carrying the expressed ERCC-1 gene.

The CHO cells transformed with the human ERCC-1 gene repaired the active DHFR gene much nore efficiently than the non-transcribed sequences, a pattern similar to that seen in wild type CHO cells. This pattern differs from that previously reported 1n CHO cells transfected with the denV gene of bacteriophage T4, in which both active and non-transcribed DNA sequences were efficiently repaired (Bohr and Hanawalt, Cardnogenesis 8: 1333–1336, 1987). The ERCC-1 gene product may specifically substitute for the repair enzyme present in normal hamster cells while the denV product, T4 endonuclease V, does not be appear to be constrained in its access to inactive chromatin.


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