The nucleotide excision repair mechanism (NER) of Escherichia coli is 
responsible for the recognition and elimination of more than twenty different 
DNA lesions. Herein, we evaluated the in vivo role of NER in the repair of DNA 
adducts generated by psoralens (mono- or bi-functional) and UV-A light (PUVA) in 
E. coli. Cultures of wild-type E. coli K12 and mutants for uvrA, uvrB, uvrC or 
uvrAC genes were treated with PUVA and cell survival was determined. In 
parallel, kinetics of DNA repair was also evaluated by the comparison of DNA 
sedimentation profiles in all the strains after PUVA treatment. The uvrB mutant 
was more sensitive to PUVA treatment than all the other uvr mutant strains. 
Wild-type strain, and uvrA and uvrC mutants were able to repair PUVA-induced 
lesions, as seen by DNA sedimentation profiles, while the uvrB mutant was unable 
to repair the lesions. In addition, a quadruple fpg nth xth nfo mutant was 
unable to nick PUVA-treated DNA when the crude cell-free extract was used to 
perform plasmid nicking. These data suggest that DNA repair of PUVA-induced 
lesions may require base excision repair functions, despite proficient UvrABC 
activity. These results point to a specific role for UvrB protein in the repair 
of psoralen adducts, which appear to be independent of UvrA or UvrC proteins, as 
described for the classical UvrABC endonuclease mechanism.