These results seem surprising, considering that one key function of the NER system is to limit mutations by repairing DNA lesions. Our results are, however, click here consistent with previous findings in E. coli, where decreased mutation frequencies were reported in uvrA and uvrB mutants after treatment with oxidized deoxyribonucleotides, while mutation rates were unaffected in a uvrC mutant [31]. Under non-damage-inducing conditions, E. coli mutants in uvrA uvrB and uvrC

exhibited a lower mutation rate [24]. The excision and replacement of undamaged bases were first characterized by Branum and colleagues who showed that in E. coli and in human cells, NER is able to excise damage-free fragments in lengths of 12–13 and 24–32 bp,

respectively [32]. This process has been referred to as “gratuitous mutations” and it has been suggested that it may be a major source of oncogene mutations in humans [15, 33]. GSK1120212 Such a double functionality of the NER proteins has been also reported for Pseudomonas putida and E. coli where the NER system is also involved in the generation of mutations [24, 34]. Based on our results, we hypothesize that the basal level of NER-mediated replacement activity on undamaged DNA is contributing to the overall high mutation frequency that is characteristic of H. pylori and contributes to its rapid genetic diversification [4, 7, 10]. As outlined above, the effects of uvrC inactivation on mutation rates in other bacterial species are complex and depend on the experimental conditions. this website We note that uvrC does not appear to contribute to the generation of gratuitous mutations in H. pylori. The NER system has a dual role in the control of the homologous recombination in H. pylori Our data show that the inactivation of uvrA significantly decreased the recombination

frequency after natural transformation of H. pylori. A decrease was also observed with a uvrB mutant, which was suggestive (BF = 14), Florfenicol but did not reach statistical significance. The recombination frequency could be restored by functional complementation, indicating that UvrA facilitates homologous recombination in H. pylori. UvrA was not essential for this process, since recombinants were still detected in the mutant. Recombination frequencies differed significantly between uvrA and uvrB mutants, the reason of this statistically highly significant difference between both mutants remains to be elucidated. Inactivation of UvrC likewise had no significant effect on recombination frequencies in H. pylori. By contrast, UvrD was found to act as an inhibitor of homologous recombination, as previously shown by other investigators [23]. We note that inactivation of uvrC promoted the incorporation of significantly longer DNA fragments into the H. pylori genome (2.2 fold increase) in comparison to the wild type strain, while a complemented mutant strain exhibited imports indistinguishable from wild type.