Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-3-22
pubmed:abstractText
Two pathways for DNA recombination, AddAB (RecBCD-like) and RecRO, were identified in Helicobacter pylori, a pathogenic bacterium that colonizes human stomachs resulting in a series of gastric diseases. In this study, we examined the physiological roles of H. pylori RecRO pathway in DNA recombinational repair. We characterized H. pylori single mutants in recR and in recO, genes in the putative gap repair recombination pathway, and an addA recO double mutant that is thus deficient in both pathways that initiate DNA recombinational repair. The recR or recO single mutants showed the same level of sensitivity to mitomycin C as the parent strain, suggesting that the RecRO pathway is not responsible for the repair of DNA double strand breaks. However, H. pylori recR and recO mutants are highly sensitive to oxidative stress and separately to acid stress, two major stress conditions that H. pylori encounters in its physiological niche. The complementation of the recR mutant restored the sensitivity to oxidative and acid stress to the wild type level. By measuring DNA transformation frequencies, the recR and recO single mutants were shown to have no effect on inter-genomic recombination, whereas the addA recO double mutant had a greatly (?12-fold) reduced transformation frequency. On the other hand, the RecRO pathway was shown to play a significant role in intra-genomic recombination with direct repeat sequences. Whereas the recA strain had a deletion frequency 35-fold lower than that of background level, inactivation of recR resulted in a 4-fold decrease in deletion frequency. In a mouse infection model, the three mutant strains displayed a greatly reduced ability to colonize the host stomachs. The geometric means of colonization number for the wild type, recR, recO, and addA recO strains were 6 x 10?, 1.6 x 10?, 1.4 x 10? and 4 x 10³ CFU/g stomach, respectively. H. pylori RecRO-mediated DNA recombinational repair (intra-genomic recombination) is thus involved in repairing DNA damage induced by oxidative and acid stresses and plays an important role in bacterial survival and persistent colonization in the host.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1568-7856
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
3
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
373-9
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:21292567-Acids, pubmed-meshheading:21292567-Animals, pubmed-meshheading:21292567-Bacterial Proteins, pubmed-meshheading:21292567-Cross-Linking Reagents, pubmed-meshheading:21292567-DNA Repair, pubmed-meshheading:21292567-Gene Order, pubmed-meshheading:21292567-Helicobacter Infections, pubmed-meshheading:21292567-Helicobacter pylori, pubmed-meshheading:21292567-Host-Pathogen Interactions, pubmed-meshheading:21292567-Metronidazole, pubmed-meshheading:21292567-Mice, pubmed-meshheading:21292567-Mice, Inbred C57BL, pubmed-meshheading:21292567-Microbial Viability, pubmed-meshheading:21292567-Mitomycin, pubmed-meshheading:21292567-Models, Animal, pubmed-meshheading:21292567-Mutation, pubmed-meshheading:21292567-Oxidative Stress, pubmed-meshheading:21292567-Radiation-Sensitizing Agents, pubmed-meshheading:21292567-Recombination, Genetic, pubmed-meshheading:21292567-Repetitive Sequences, Nucleic Acid, pubmed-meshheading:21292567-Stomach, pubmed-meshheading:21292567-Ultraviolet Rays
pubmed:year
2011
pubmed:articleTitle
The RecRO pathway of DNA recombinational repair in Helicobacter pylori and its role in bacterial survival in the host.
pubmed:affiliation
Department of Microbiology, 815 Biological Sciences Building, University of Georgia, Athens, GA 30602, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural