BMC Microbiology | |
The nucleotide excision repair (NER) system of Helicobacter pylori: Role in mutation prevention and chromosomal import patterns after natural transformation | |
Research Article | |
Xavier Didelot1  Christian Kraft2  Christelle Bahlawane2  Claudia Moccia2  Juliane Krebes2  Stefan Kulick2  Sebastian Suerbaum2  | |
[1] Department of Statistics, University of Oxford, 1 South Parks Road, OX1 3TG, Oxford, UK;Institute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany; | |
关键词: Helicobacter pylori; Mutation; Recombination; Nucleotide excision repair; | |
DOI : 10.1186/1471-2180-12-67 | |
received in 2012-02-08, accepted in 2012-04-24, 发布年份 2012 | |
来源: Springer | |
【 摘 要 】
BackgroundExtensive 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.ResultsInactivation 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.ConclusionsOur 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】
Unknown
© Moccia et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
【 预 览 】
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