Transcription-coupled DNA repair (TCR) is a subpathway of nucleotide excision 
repair (NER) that is triggered when RNA polymerase is stalled by DNA damage. 
Lesions targeted by TCR are repaired more quickly than lesions repaired by the 
transcription-independent "global" NER pathway, but the mechanism underlying 
this rate enhancement is not understood. Damage recognition during bacterial NER 
depends upon UvrA, which binds to the damage and loads UvrB onto the DNA. 
Bacterial TCR additionally requires the Mfd protein, a DNA translocase that 
removes the stalled transcription complexes. We have determined the properties 
of Mfd, UvrA, and UvrB that are required for the elevated rate of repair 
observed during TCR. We show that TCR and global NER differ in their 
requirements for damage recognition by UvrA, indicating that Mfd acts at the 
very earliest stage of the repair process and extending the functional 
similarities between TCR in bacteria and eukaryotes.