DNA damage is preferentially repaired in the transcribed strand of many active 
genes. Although the concept of DNA repair coupled with transcription has been 
widely accepted, its mechanisms remain elusive. We recently reported that in 
Chinese hamster ovary cells while ultraviolet light-induced cyclobutane 
pyrimidine dimers (CPDs) are preferentially repaired in the transcribed strand 
of dihydrofolate reductase gene, CPDs are efficiently repaired in both strands 
of adenine phosphoribosyltransferase (APRT) locus, in either a transcribed or 
nontranscribed APRT gene (1). These results suggested that the transcription 
dependence of repair may depend on genomic context. To test this hypothesis, we 
constructed transfectant cell lines containing a single, actively transcribed 
APRT gene, integrated at different genomic sites. Mapping of CPD repair in the 
integrated APRT genes in three transfectant cell lines revealed two distinct 
repair patterns, either preferential repair of CPDs in the transcribed strand or 
very poor repair in both strands. Similar kinetics of micrococcal nuclease 
digestion were seen for all three transfectant APRT gene domains and endogenous 
APRT locus. Our results suggest that both the efficiency and strand-specificity 
of repair of an actively transcribed gene are profoundly affected by genomic 
context but do not reflect changes in first order nucleosomal structure.