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. 1991 Oct 25;19(20):5633-7.
doi: 10.1093/nar/19.20.5633.

Induction of a mutant phenotype in human repair proficient cells after overexpression of a mutated human DNA repair gene

P B Belt  1 , M F van Oosterwijk, H Odijk, J H Hoeijmakers, C Backendorf
Affiliations
Free PMC article

Induction of a mutant phenotype in human repair proficient cells after overexpression of a mutated human DNA repair gene

P B Belt et al. Nucleic Acids Res. .
Free PMC article

Abstract

Antisense and mutated cDNA of the human excision repair gene ERCC-1 were overexpressed in repair proficient HeLa cells by means of an Epstein-Barr-virus derived cDNA expression vector. Whereas antisense RNA did not influence the survival of the transfected cells, a mutated cDNA generating an ERCC-1 protein with two extra amino acids in a conserved region of its C-terminal part resulted in a significant sensitization of the HeLa transfectants to mitomycin C-induced damage. These results suggest that overexpression of the mutated ERCC-1 protein interferes with proper functioning of the excision repair pathway in repair proficient cells and is compatible with a model in which the mutated ERCC-1 protein competes with the wild-type polypeptide for a specific step in the repair process or for occupation of a site in a repair complex. Apparently, this effect is more pronounced for mitomycin C induced crosslink repair than for UV-induced DNA damage.

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