Genome-Wide Transcriptional Profiling in a Histidine Kinase Mutant of
            <i>Helicobacter pylori</i>
            Identifies Members of a Regulon

Forsyth, Mark H.; Cao, Ping; Garcia, Preston P.; Hall, Joshua D.; Cover, Timothy L.

doi:10.1128/jb.184.16.4630-4635.2002

Cited by 46 publications

(55 citation statements)

References 17 publications

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“…The observation that the histidine kinase gene hp165 is not essential suggests that there are two sets of target genes of HP166; one group is essential for viability and is controlled by unphosphorylated HP166, while the second group is nonessential and is regulated by the phosphorylated response regulator (HP166ϳP). Target genes whose regulation requires HP166ϳ P have been identified previously (10,12,32). In this study we demonstrated by genetic complementation that the essential function of HP166 can be provided by a mutated response regulator derivative which is not capable of phosphorylation.…”

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confidence: 82%

“…The NtrC-like response regulator HP703 controls the transcription of genes encoding components of the flagellar basal body and hook and the minor flagellin FlaB (35). In response to an acidic pH HP166 regulates the expression of the urease genes and of several genes encoding H. pylori-specific proteins with unknown functions (10,12,32). On the basis of in vitro DNA-binding experiments, it was hypothesized that HP1043 regulates its own expression, as well as transcription of the tlpB gene encoding a methyl-accepting chemotaxis protein (9).…”

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confidence: 99%

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Phosphorylation-Independent Activity of Atypical Response Regulators ofHelicobacter pylori

Schär

Sickmann²,

Beier

2005

J Bacteriol

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The genome of the gastric pathogen Helicobacter pylori harbors a remarkably low number of regulatory genes, including three and five open reading frames encoding two-component histidine kinases and response regulators, respectively, which are putatively involved in transcriptional regulation. Two of the response regulator genes, hp1043 and hp166, proved to be essential for cell growth, and inactivation of the response regulator gene hp1021 resulted in a severe growth defect, as indicated by a small-colony phenotype. The sequences of the receiver domains of response regulators HP1043 and HP1021 differ from the consensus sequence of the acidic pocket of the receiver domain which is involved in the phosphotransfer reaction from the histidine kinase to the response regulator. Using a genetic complementation system, we demonstrated that the function of response regulator HP166, which is essential for cell growth, can be provided by a mutated derivative carrying a D52N substitution at the site of phosphorylation. We found that the atypical receiver sequences of HP1043 and HP1021 are not crucial for the function of these response regulators. Phosphorylation of the receiver domains of HP1043 and HP1021 is not needed for response regulator function and may not occur at all. Thus, the phosphorylation-independent action of these regulators differs from the well-established two-component paradigm.

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confidence: 82%

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confidence: 99%

Phosphorylation-Independent Activity of Atypical Response Regulators ofHelicobacter pylori

Schär

Sickmann²,

Beier

2005

J Bacteriol

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“…These two strains, both from Caucasian males, are closely matched in DNA sequences flanking the ins180 site, which suggested that this element might be a useful marker for distinguishing different types of strains. In addition, jhp0152 and the downstream jhp0151 genes are coexpressed from a single promoter (10,17), and ins180 is approximately 125 bp upstream of the transcriptional start site of jhp0152. We hypothesize that ins180 may introduce or disrupt a cis-acting sequence that affects downstream gene transcription.…”

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confidence: 99%

Novel 180- and 480-Base-Pair Insertions in African and African-American Strains of Helicobacter pylori

et al. 2004

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Helicobacter pylori is a genetically diverse bacterial species that chronically infects human stomachs and sometimes causes severe gastroduodenal disease. Studies of polymorphic DNA sequences can suggest geographic origins of individual strains. Here, we describe a 180-bp insertion (ins180), which is just after the translation stop of a gene of unknown function, near the promoter of jhp0152-jhp0151 two-component signal transduction genes in strain J99, and absent from this site in strain 26695. This ins180 insertion was found in 9 of 9 Gambian (West African), 9 of 20 (45%) South African, and 9 of 40 (23%) Spanish strains but in only 2 of 20 (10%) North American strains and none of 20 Lithuanian, 20 Indian, and 20 Japanese strains. Four South African isolates that lacked ins180 and that belonged to an unusual outlier group contained a 480-bp insertion at this site (ins480), whereas none of 181 other strains screened contained ins480. In further tests 56% (10 of 18) of strains from African Americans but only 17% (3 of 18) of strains from Caucasian Americans carried ins180 (P < 0.05). Thus, the H. pylori strains of modern African Americans seem to retain traces of African roots, despite the multiple generations since their ancestors were taken from West Africa. Fragmentary ins180-like sequences were found at numerous sites in H. pylori genomes, always between genes. Such sequences might affect regulation of transcription and could facilitate genome rearrangement by homologous recombination. Apparent differences between African-American and Caucasian-American H. pylori gene pools may bear on our understanding of H. pylori transmission and disease outcome.

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“…Whole-genome transcriptional profiling of H. pylori strains cultured in low pH conditions identified more than 100 genes that were differentially expressed in the wild-type strain compared with an ArsS-deficient mutant (17). Transcriptional profiling of H. pylori cultured in neutral pH conditions identified a smaller number of genes that were differentially expressed in the wild-type and ArsS null mutant strains (26). Acid-responsive H. pylori genes that are differentially expressed in wild-type and arsS mutant strains include amidases (amiE, amiF) and members of the urease gene cluster (ureA, ureB, ureE, ureF, ureG, ureH, and ureI) (9, 10, 16 -18).…”

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“…A second set of genes in the ArsR regulon is not required for cell viability, and the regulation of these genes occurs by a pathway involving a phosphorylated form of ArsR (i.e. requiring the cognate histidine kinase, ArsS) (13,17,18,20,26,29 …”

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Structural Analysis of the DNA-binding Domain of the Helicobacter pylori Response Regulator ArsR

Gupta¹,

Borin²,

Cover

et al. 2009

Journal of Biological Chemistry

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Genome-Wide Transcriptional Profiling in a Histidine Kinase Mutant of Helicobacter pylori Identifies Members of a Regulon

Cited by 46 publications

References 17 publications

Phosphorylation-Independent Activity of Atypical Response Regulators ofHelicobacter pylori

Phosphorylation-Independent Activity of Atypical Response Regulators ofHelicobacter pylori

Novel 180- and 480-Base-Pair Insertions in African and African-American Strains of Helicobacter pylori

Structural Analysis of the DNA-binding Domain of the Helicobacter pylori Response Regulator ArsR

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