Transcription-coupled nucleotide excision repair (TC-NER) removes certain kinds 
of lesions from the transcribed strand of expressed genes. The signal for TC-NER 
is thought to be RNA polymerase stalled at a lesion in the DNA template. In 
Escherichia coli, the stalled polymerase is dissociated from the lesion by the 
transcription repair coupling factor (Mfd protein), which also recruits excision 
repair proteins to the site resulting in efficient removal of the lesion. TC-NER 
has been documented in cells from a variety of organisms ranging from bacteria 
to humans. In each case, the RNA polymerase involved has been a multimeric 
protein complex. To ascertain whether a gene transcribed by the monomeric RNA 
polymerase of bacteriophage T7 could be repaired by TC-NER, we constructed 
strains of E. coli in which the chromosomal lacZ gene is controlled by a T7 
promoter. In the absence of T7 RNA polymerase, little or no beta-galactosidase 
is produced, indicating that the E. coli RNA polymerase does not transcribe lacZ 
efficiently, if at all, in these strains. By introducing a plasmid (pAR1219) 
carrying the T7 gene 1 under control of the E. coli lac UV5 promoter into these 
strains, we obtained derivatives in which the level of T7 RNA polymerase could 
be regulated. In cultures containing upregulated levels of the polymerase, 
beta-galactosidase was actively produced indicating that the T7 RNA polymerase 
transcribes the lacZ gene efficiently. Under these conditions, we observed that 
UV-induced cyclobutane pyrimidine dimers were removed more rapidly from the 
transcribed strand of lacZ than from the nontranscribed strand, supporting the 
conclusion that TC-NER occurred in this gene. This response was absent in an 
mfd-1 mutant, indicating that the underlying mechanism may be similar to that 
for the bacterial RNA polymerase.