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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.

bmc microbiology

The nucleotide excision repair (NER) system of Helicobacter pylori: Role in mutation prevention and chromosomal import patterns after natural transformation