In humans, DNA lesions such as pyrimidine dimers in the template strand of genes 
transcribed by RNA polymerase II are repaired faster than those in the coding 
strand and nontranscribed regions of the genome. This phenomenon, referred to as 
transcription-coupled repair (i) requires active transcription, (ii) does not 
require the XPC gene product which is essential for general/basal repair 
reactions, and (iii) requires the CSA and CSB proteins. We have developed an in 
vitro model system that consists of purified human excision repair factors and a 
DNA substrate analogous to a transcription bubble terminating at a cyclobutane 
thymine dimer. In this system the thymine dimer was excised independent of XPC. 
Furthermore, the thymine dimer in the bubble-containing substrate was removed 
approximately 3-fold faster by the excision repair nuclease reconstituted with 
or without XPC, compared with the removal of thymine dimer from a base paired 
duplex by the entire set of excision nuclease factors. These results provide 
important insight into the mechanism of transcription-coupled repair in humans.