Open Access Highly Accessed Research article

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

Claudia Moccia1, Juliane Krebes1, Stefan Kulick1, Xavier Didelot2, Christian Kraft1, Christelle Bahlawane1 and Sebastian Suerbaum1*

Author Affiliations

1 Institute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Carl-Neuberg-Str. 1, , 30625, Hannover, Germany

2 Department of Statistics, University of Oxford, 1 South Parks Road, Oxford, OX1 3TG, UK

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BMC Microbiology 2012, 12:67  doi:10.1186/1471-2180-12-67

Published: 6 May 2012



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.


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.


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.

Helicobacter pylori; Mutation; Recombination; Nucleotide excision repair