Transcription-coupled repair (TCR) is a subpathway of nucleotide excision repair 
(NER) that acts specifically on lesions in the transcribed strand of expressed 
genes. First reported in mammalian cells, TCR was then documented in Escherichia 
coli. In this organism, an RNA polymerase arrested at a lesion is displaced by 
the transcription repair coupling factor, Mfd. This protein recruits the NER 
lesion-recognition factor UvrA, and then dissociates from the DNA. UvrA binds 
UvrB, and the assembled UvrAB* complex initiates repair. In mutants lacking 
active Mfd, TCR is absent. A gene transcribed by the bacteriophage T7 RNA 
polymerase in E. coli also requires Mfd for TCR. The CSB protein (missing or 
defective in cells of patients with Cockayne syndrome, complementation group B) 
is essential for TCR in humans. CSB and its homologs in higher eukaryotes are 
likely functional equivalents of Mfd.