Growth Phase Regulation of
 flaA
 Expression in
 Helicobacter pylori
 Is
 luxS
 Dependent

Loh, John T.; Forsyth, Mark H.; Cover, Timothy L.

doi:10.1128/iai.72.9.5506-5510.2004

Cited by 41 publications

(45 citation statements)

References 36 publications

(34 reference statements)

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“…Furthermore, in their studies, maximal accumulation of AI-2 in the culture occurred in stationary phase. It has also been reported that the expression of H. pylori flaA is growth-phase dependent (Thompson et al, 2003), and that flaA transcription increases with culture density (Loh et al, 2004) at stationary phase. Mutating the luxS gene eliminates the growth-phase dependence of flaA, and growth-phase dependence is restored when the luxS mutant is complemented with wild-type luxS.…”

Section: Introductionmentioning

confidence: 88%

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Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Osaki¹,

Hanawa²,

Manzoku³

et al. 2006

Journal of Medical Microbiology

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Helicobacter pylori is associated with gastric disorders in humans and some experimental animals, and possesses the luxS/type 2 autoinducer (AI-2) system. The effects of a specific luxS mutation on the characteristics of H. pylori were examined. On 0?3 % agar medium, motility of H. pylori HPKY08 (luxS : : cat) was significantly lower than that of wild-type H. pylori TK1402. The luxS-complemented strain HPKY21 exhibited motility comparable to that of H. pylori TK1402. It was shown that the luxS/AI-2 system plays an important role in H. pylori motility. The luxS mutant exhibited a reduced infection rate relative to the wild-type parent strain TK1402 in a Mongolian gerbil model. At 3 months after oral inoculation, lower numbers of H. pylori were detected by semi-quantitative real-time reverse transcription PCR (qRT-PCR) in luxS " mutant-infected gerbils than in TK1402-infected gerbils. Gastric inflammation and increased antibody titre for H. pylori were observed in TK1402-infected gerbils only. INTRODUCTIONQuorum sensing (QS) is a cell-to-cell communication system that regulates bacterial phenotypes, including the expression of virulence factor genes. The signalling molecules are known as autoinducers (AIs), and when these molecules reach a critical threshold concentration within a bacterial population, a signal transduction cascade is triggered, and this forms the basis for alterations in gene expression (Fuqua et al., 1994). Many Gram-negative bacteria utilize N-acylhomoserine lactone molecules, AI-1, as signals, while Gram-positive bacteria actively export peptides as signalling molecules. There is a second signalling system involved in a wide range of bacterial species (Schauder et al., 2001), and this system is utilized by both Gram-positive and Gram-negative bacteria. The signalling molecule known as type 2 autoinducer (AI-2) is a furanosyl borate diester (Chen et al., 2002), and the enzyme responsible for its synthesis is encoded by the luxS gene (Surette & Bassler, 1999). The genomes of many bacterial species, notably Escherichia coli, Salmonella enterica serovar Typhimurium, Shigella flexneri, Proteus mirabilis, Vibrio cholerae, Vibrio vulnificus, Campylobacter jejuni, Porphyromonas gingivalis, Bacillus subtilis, Streptococcus pyogenes, Streptococcus mutans, Clostridium perfringens and Clostridium difficile, include luxS homologues. In several of these, luxS-related AI-2 signals are involved in bacterial characteristics such as biofilm formation (Balestrino et al., 2005;Blehert et al., 2003;Fong et al., 2001;Wen & Burne 2004), flagella and motility (Jeon et al., 2003;Schneider et al., 2002;Stroeher et al., 2003), type III secretion systems (Sperandio et al., 1999), toxin production (Ohtani et al., 2002) and virulence (Lyon et al., 2001; Parsonnet et al., 1991;Stroeher et al., 2003).Helicobacter pylori has been identified as the aetiological agent of chronic active gastritis, peptic ulcer disease (Blaser, 1992;Graham, 1989), gastric adenocarcinoma (Parsonnet et al., 1991) and mucosal-associated lymphoid t...

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Section: Introductionmentioning

confidence: 88%

“…The present study is the first to show significantly reduced motility of the H. pylori luxS mutant. Recently, it has been shown that mutating the H. pylori luxS gene eliminates growth-phase-dependent control of flaA (Loh et al, 2004). …”

Section: Growth Of Luxs Mutantmentioning

confidence: 99%

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Osaki¹,

Hanawa²,

Manzoku³

et al. 2006

Journal of Medical Microbiology

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“…Expression of early flagellar genes generally requires a transcriptional activator, referred to as the master regulator. While a master regulator has yet to be identified in H. pylori, some studies have shown that the quorum-sensing autoinducer synthase LuxS affects motility by altering expression of early and late flagellar genes (Loh et al, 2004;Osaki et al, 2006;Rader et al, 2007). The effect of LuxS on flagellar gene expression, however, is strainspecific (Joyce et al, 2000;Lee et al, 2006), and may be due to global changes in gene expression caused by decreased fitness in the luxS mutant rather than loss of quorum sensing (Lee et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori FlhB processing-deficient variants affect flagellar assembly but not flagellar gene expression

2009

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Regulation of the Helicobacter pylori flagellar gene cascade involves the transcription factors s 54 (RpoN), employed for expression of genes required midway through flagellar assembly, and s 28 (FliA), required for expression of late genes. Previous studies revealed that mutations in genes encoding components of the flagellar protein export apparatus block expression of the H. pylori RpoN and FliA regulons. FlhB is a membrane-bound component of the export apparatus that possesses a large cytoplasmic domain (FlhB C ). The hook length control protein FliK interacts with FlhB C to modulate the substrate specificity of the export apparatus. FlhB C undergoes autocleavage as part of the switch in substrate specificity. Consistent with previous reports, deletion of flhB in H. pylori interfered with expression of RpoN-dependent reporter genes, while deletion of fliK stimulated expression of these reporter genes. In the DflhB mutant, disrupting fliK did not restore expression of RpoN-dependent reporter genes, suggesting that the inhibitory effect of the DflhB mutation is not due to the inability to export FliK. Amino acid substitutions (N265A and P266G) at the putative autocleavage site of H. pylori FlhB prevented processing of FlhB and export of filament-type substrates. The FlhB variants supported wild-type expression of RpoN-and FliA-dependent reporter genes. In the strain producing FlhB N265A , expression of RpoN-and FliA-dependent reporter genes was inhibited when fliK was disrupted. In contrast, expression of these reporter genes was unaffected or slightly stimulated when fliK was disrupted in the strain producing FlhB P266G. H. pylori HP1575 (FlhX) shares homology with the C-terminal portion of FlhB C (FlhB CC ) and can substitute for FlhB CC in flagellar assembly. Disrupting flhX inhibited expression of a flaB reporter gene in the wild-type but not in the DfliK mutant or strains producing FlhB variants, suggesting a role for FlhX or FlhB CC in normal expression of the RpoN regulon. Taken together, these data indicate that the mechanism by which the flagellar protein export apparatus exerts control over the H. pylori RpoN regulon is complex and involves more than simply switching substrate specificity of the flagellar protein export apparatus. INTRODUCTIONBacterial flagellar biosynthesis involves transcriptional hierarchies that coordinate flagellar gene expression with assembly. Flagellar gene hierarchies are well characterized in a few bacteria, including Salmonella enterica serovar Typhimurium (S. typhimurium) and Caulobacter crescentus (Chilcott & Hughes, 2000;Wu & Newton, 1997). Flagellar gene regulation in e-Proteobacteria, such as Helicobacter pylori and Campylobacter jejuni, shares some similarities with these established paradigms but also differs significantly. As in S. typhimurium, H. pylori flagellar genes required late in assembly, such as the major flagellin (FlaA) and filament cap protein, are transcribed by s 28 (FliA)-RNA polymerase holoenzyme (Kim et al., 1999;Leying et al., 1992), and, as in C....

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“…As a result, AI-2 has been suggested to represent a widely distributed quorum-sensing signal that is recognized by many organisms (39). Inactivation of luxS has been reported to influence a wide variety of cellular processes, including type III secretion (43), cell motility (26,42), the development of biofilms (4,8,17,18,29,30,56), the expression of virulence factors (12,22,28), and iron uptake (11). The signal transduction mechanism that governs the cellular response to AI-2 has been most thoroughly characterized in Vibrio spp.…”

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confidence: 99%

Autoinducer 2 Is Required for Biofilm Growth ofAggregatibacter(Actinobacillus)actinomycetemcomitans

2007

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Autoinducer 2 (AI-2) is required for the growth of Aggregatibacter (Actinobacillus) actinomycetemcomitans in culture under conditions of iron limitation. However, in vivo this organism thrives in a complex multispecies biofilm that forms in the human oral cavity. In this report, we show that adherent growth of A. actinomycetemcomitans on a saliva-coated surface, but not planktonic growth under iron-replete conditions, is defective in a LuxS-deficient background. Biofilm growth of the luxS mutant exhibited lower total biomass and lower biofilm depth than those for the wild-type strain. Normal biofilm growth of the luxS mutant was restored genetically by introduction of a functional copy of luxS and biochemically by addition of partially purified AI-2. Furthermore, introduction of S-adenosylhomocysteine hydrolase, which restores the metabolism of S-adenosylmethionine in the absence of LuxS, into A. actinomycetemcomitans did not complement the luxS mutation unless AI-2 was added in trans. This suggests that AI-2 itself is required for biofilm growth by A. actinomycetemcomitans. A biofilm growth deficiency similar to that of the LuxS-deficient strain was also observed when a gene encoding the AI-2-interacting protein RbsB or LsrB was inactivated. Biofilm formation by A. actinomycetemcomitans was virtually eliminated upon inactivation of both rbsB and lsrB. In addition, biofilm growth by wild-type A. actinomycetemcomitans was reduced in the presence of ribose, which competes with AI-2 for binding to RbsB. These results suggest that RbsB and LsrB function as AI-2 receptors in A. actinomycetemcomitans and that the development of A. actinomycetemcomitans biofilms requires AI-2.

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Growth Phase Regulation of flaA Expression in Helicobacter pylori Is luxS Dependent

Cited by 41 publications

References 36 publications

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Helicobacter pylori FlhB processing-deficient variants affect flagellar assembly but not flagellar gene expression

Autoinducer 2 Is Required for Biofilm Growth ofAggregatibacter(Actinobacillus)actinomycetemcomitans

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