BACKGROUND: Extensive genetic diversity and rapid allelic diversification are 
characteristics of the human gastric pathogen Helicobacter pylori, and are 
believed to contribute to its ability to cause chronic infections. Both a high 
mutation rate and frequent imports of short fragments of exogenous DNA during 
mixed infections play important roles in generating this allelic diversity. In 
this study, we used a genetic approach to investigate the roles of nucleotide 
excision repair (NER) pathway components in H. pylori mutation and 
recombination.
RESULTS: Inactivation of any of the four uvr genes strongly increased the 
susceptibility of H. pylori to DNA damage by ultraviolet light. Inactivation of 
uvrA and uvrB significantly decreased mutation frequencies whereas only the uvrA 
deficient mutant exhibited a significant decrease of the recombination frequency 
after natural transformation. A uvrC mutant did not show significant changes in 
mutation or recombination rates; however, inactivation of uvrC promoted the 
incorporation of significantly longer fragments of donor DNA (2.2-fold increase) 
into the recipient chromosome. A deletion of uvrD induced a 
hyper-recombinational phenotype.
CONCLUSIONS: Our data suggest that the NER system has multiple functions in the 
genetic diversification of H. pylori, by contributing to its high mutation rate, 
and by controlling the incorporation of imported DNA fragments after natural 
transformation.