Transcription-coupled repair (TCR) and global genomic repair (GGR) of UV-induced 
cyclobutane pyrimidine dimers were investigated in the yeast GAL1-10 genes. Both 
Rpb9- and Rad26-mediated TCR are confined to the transcribed strands, initiating 
at upstream sites approximately 100 nucleotides from the upstream activating 
sequence shared by the two genes. However, TCR initiation sites do not correlate 
with either transcription start sites or TATA boxes. Rad16-mediated GGR tightly 
correlates with nucleosome positioning when the genes are repressed and are slow 
in the nucleosome core and fast in linker DNA. Induction of transcription 
enhanced GGR in nucleosome core DNA, especially in the nucleosomes around and 
upstream of the transcription start sites. Furthermore, when the genes were 
induced, GGR was slower in the transcribed regions than in the upstream regions. 
Finally, simultaneous deletion of RAD16, RAD26, and RPB9 resulted in no 
detectable repair in all sites along the region analyzed. Our results suggest 
that (a). TCR may be initiated by a transcription activator, presumably through 
the loading of RNA polymerase II, rather than by transcription initiation or 
elongation per se; (b). TCR and nucleosome disruption-enhanced GGR are the major 
causes of rapid repair in regions around and upstream of transcription start 
sites; (c). transcription machinery may hinder access of NER factors to a DNA 
lesion in the absence of a transcription-repair coupling factor; and (d). other 
than GGR mediated by Rad16 and TCR mediated by Rad26 and Rpb9, no other 
nucleotide excision repair pathway exists in these RNA polymerase II-transcribed 
genes.