Murine DNA repair gene located on chromosome 4.

Xeroderma pigmentosum (XP) is an autosomal recessive human disease in which affected individuals are prone to develop skin cancers after exposure to sunlight. Cells from XP patients are defective in DNA repair activity and are sensitive to UV light. Most XP individuals have a defect in the excision repair pathway for UV damage. Genetic studies have indicated that excision-defective cells fall into seven complementation groups (A-G). An eighth group of XP is known to be defective in post-replication repair. DNA repair enzymes are ubiquitous and can function across species boundaries. Primary mouse embryo fibroblasts have normal levels of DNA repair functions. We report here that somatic cell hybrids between primary mouse cells and SV40-transformed XP group A cells can express wild-type levels of DNA repair function. These hybrid cells segregate murine chromosomes in culture. The proportion of cells in a given hybrid cell line which can perform unscheduled DNA synthesis (UDS) correlated well with the percentage of the population retaining murine chromosome 4. This study presents the first example of a direct quantitative comparison of specific gene activity and chromosomal content on a cellular basis.