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

BMC Microbiology

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

[1] Institute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Carl-Neuberg-Str. 1, , 30625, Hannover, Germany;Department of Statistics, University of Oxford, 1 South Parks Road, Oxford, OX1 3TG, UK

关键词: Nucleotide excision repair;    Recombination;    Mutation;    Helicobacter pylori;   

Others  :  1221958
DOI  :  10.1186/1471-2180-12-67

 received in 2012-02-08, accepted in 2012-04-24,  发布年份 2012

【 摘 要 】

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.

【 授权许可】

   
2012 Moccia et al.; licensee BioMed Central Ltd.

【 图 表 】

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