Restriction–modification system differences in <i>Helicobacter pylori</i> are a barrier to interstrain plasmid transfer

Ando, Takafumi; Xu, Qing; Torres, Melaine; Kusugami, Kazuo; Israel, Dawn A.; Blaser, Martin J.

doi:10.1046/j.1365-2958.2000.02049.x

Cited by 127 publications

(88 citation statements)

References 54 publications

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“…These are more difficult to assay biochemically. These findings of multiple active M genes without corresponding R genes reinforces previous warnings that restriction cannot be assumed just because site-specific modifications are found (28).…”

Section: Discussionsupporting

confidence: 86%

Comparative genomics of the restriction-modification systems in Helicobacter pylori

Lin

Pósfai

Roberts

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

153

164

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Helicobacter pylori is a Gram-negative bacterial pathogen with a small genome of 1.64 -1.67 Mb. More than 20 putative DNA restrictionmodification (R-M) systems, comprising more than 4% of the total genome, have been identified in the two completely sequenced H. pylori strains, 26695 and J99, based on sequence similarities. In this study, we have investigated the biochemical activities of 14 Type II R-M systems in H. pylori 26695. Less than 30% of the Type II R-M systems in 26695 are fully functional, similar to the results obtained from strain J99. Although nearly 90% of the R-M genes are shared by the two H. pylori strains, different sets of these R-M genes are functionally active in each strain. Interestingly, all strain-specific R-M genes are active, whereas most shared genes are inactive. This agrees with the notion that strain-specific genes have been acquired more recently through horizontal transfer from other bacteria and selected for function. Thus, they are less likely to be impaired by random mutations. Our results also show that H. pylori has extremely diversified R-M systems in different strains, and that the diversity may be maintained by constantly acquiring new R-M systems and by inactivating and deleting the old ones.H elicobacter pylori is one of the most common bacterial pathogens that colonizes the gastric mucosa of humans. H. pylori is implicated in a wide range of gastroduodenal diseases (1, 2). H. pylori is commonly believed to be a very diverse species. It is believed that, in addition to genetic recombination, de novo mutation could have a role in generating the high level of genetic variation in H. pylori (3). MutH and MutL homologues cannot be found in H. pylori genomes, which suggests H. pylori may not have a functional mismatch repair system (4, 5). Recent analysis of the complete genomic sequences of two unrelated H. pylori isolates reveals that although intraspecies variation does exist, the overall genomic organization, gene order, and predicted proteins of the two strains are quite similar (5, 6). Approximately 6-7% of the genes are specific to each strain (5). The 26695 and J99 strains have a relatively small genome size of 1.67 and 1.64 megabase pairs (4, 5). However, more than twenty DNA restriction-modification (R-M) systems can be identified in each strain based on sequence similarities. The biological significance of this large complement of R-M systems is not clear. The majority of the H. pylori R-M systems are of Type II, which consist of two separate enzymes: the restriction endonucleases, which are responsible for degrading unmodified foreign DNA, and the modification DNA methyltransferases (methylase or M), which protect endogenous DNA from endonucleolytic digestion by methylating them at the endonuclease recognition sites (7).Interesting observations have been reported regarding H. pylori R-M genes. A novel H. pylori gene, iceA (induced when the bacteria contact the host epithelium), was identified recently (8). DNA sequences have revealed two alleles of the iceA locu...

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Section: Discussionsupporting

confidence: 86%

Comparative genomics of the restriction-modification systems in Helicobacter pylori

Lin

Pósfai

Roberts

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

153

164

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“…A total of 153 strain-specific genes (98 B128-specific and 55 G1.1-specific; Figure 4) were identified in the two isolates, and 44 (29%) of these (Table 1) were predicted to encode gene products with known, diverse functions such as recombination (xerD) and basic cellular metabolism (yxjE, trpA, topA3). A substantial proportion of these ORFs had significant homology to genes encoding putative restriction-modification (R-M) enzymes ( Table 1), findings that substantiate recent reports (34)(35)(36) demonstrating the presence of unique complements of R-M systems within individual H. pylori strains. The microarray also identified major differences in gene content that localize to regions of linked genes, one of which includes a portion of the cag pathogenicity island (Figure 4).…”

supporting

confidence: 80%

Helicobacter pylori strain-specific differences in genetic content, identified by microarray, influence host inflammatory responses

Salama²,

et al. 2001

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“…Transformation of C. jejuni was performed as described previously (47), with some modifications to overcome the restriction barrier of C. jejuni (5,31,49,50), following the method of Donahue (15). Briefly, bacterial cells grown on Mueller-Hinton agar for 6 h were pelleted, and then the pellet was resuspended in 5 volumes of extraction buffer (20 mM Tris-acetate [pH 7.9], 50 mM potassium acetate, 5 mM Na 2 EDTA, 1 mM DTT, protease inhibitor cocktail) and sonicated on ice.…”

Section: Methodsmentioning

confidence: 99%

The Iron-Binding Protein Dps Confers Hydrogen Peroxide Stress Resistance to Campylobacter jejuni

Ishikawa¹,

Mizunoe²,

et al. 2003

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whereas it did not appear to bind DNA. An isogenic dps-deficient mutant was more vulnerable to hydrogen peroxide than its parental strain, as judged by growth inhibition tests. The iron chelator Desferal restored the resistance of the Dps-deficient mutant to hydrogen peroxide, suggesting that this iron-binding protein prevented generation of hydroxyl radicals via the Fenton reaction. Dps was constitutively expressed during both exponential and stationary phase, and no induction was observed when the cells were exposed to H 2 O 2 or grown under iron-supplemented or iron-restricted conditions. On the basis of these data, we propose that this iron-binding protein in C. jejuni plays an important role in protection against hydrogen peroxide stress by sequestering intracellular free iron and is expressed constitutively to cope with the harmful effect of hydrogen peroxide stress on this microaerophilic organism without delay.

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Restriction–modification system differences in Helicobacter pylori are a barrier to interstrain plasmid transfer

Cited by 127 publications

References 54 publications

Comparative genomics of the restriction-modification systems in Helicobacter pylori

Comparative genomics of the restriction-modification systems in Helicobacter pylori

Helicobacter pylori strain-specific differences in genetic content, identified by microarray, influence host inflammatory responses

The Iron-Binding Protein Dps Confers Hydrogen Peroxide Stress Resistance to Campylobacter jejuni

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