Transcription-coupled repair (TCR) is a cellular process by which some forms of 
DNA damage are repaired more rapidly from transcribed strands of active genes 
than from nontranscribed strands or the overall genome. In humans, the TCR 
coupling factor, CSB, plays a critical role in restoring transcription following 
both UV-induced and oxidative DNA damage. It also contributes indirectly to the 
global repair of some forms of oxidative DNA damage. The Escherichia coli 
homolog, Mfd, is similarly required for TCR of UV-induced lesions. However, its 
contribution to the restoration of transcription and to global repair of 
oxidative damage has not been examined. Here, we report the first direct study 
of transcriptional recovery following UV-induced and oxidative DNA damage in E. 
coli. We observed that mutations in mfd or uvrA reduced the rate that 
transcription recovered following UV-induced damage. In contrast, no difference 
was detected in the rate of transcription recovery in mfd, uvrA, fpg, nth, or 
polB dinB umuDC mutants relative to wild-type cells following oxidative damage. 
mfd mutants were also fully resistant to hydrogen peroxide (H(2)O(2)) and 
removed oxidative lesions from the genome at rates comparable to wild-type 
cells. The results demonstrate that Mfd promotes the rapid recovery of gene 
expression following UV-induced damage in E. coli. In addition, these findings 
imply that Mfd may be functionally distinct from its human CSB homolog in that 
it does not detectably contribute to the recovery of gene expression or global 
repair following oxidative damage.