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PMID:10722597

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Citation

Foynes, S, Dorrell, N, Ward, SJ, Stabler, RA, McColm, AA, Rycroft, AN and Wren, BW (2000) Helicobacter pylori possesses two CheY response regulators and a histidine kinase sensor, CheA, which are essential for chemotaxis and colonization of the gastric mucosa. Infect. Immun. 68:2016-23

Abstract

Infection of the mucous layer of the human stomach by Helicobacter pylori requires the bacterium to be motile and presumably chemotactic. Previous studies have shown that fully functional flagella are essential for motility and colonization, but the role of chemotaxis remains unclear. The two-component regulatory system CheA/CheY has been shown to play a major role in chemotaxis in other enteric bacteria. Scrutiny of the 26695 genome sequence suggests that H. pylori has two CheY response regulators: one a separate protein (CheY1) and the other (CheY2) fused to the histidine kinase sensor CheA. Defined deletion mutations were introduced into cheY1, cheY2, and cheA in H. pylori strains N6 and SS1. Video tracking revealed that the wild-type H. pylori strain moves in short runs with frequent direction changes, in contrast to movement of cheY2, cheAY2, and cheAY2 cheY1 mutants, whose motion was more linear. The cheY1 mutant demonstrated a different motility phenotype of rapid tumbling. All mutants had impaired swarming and greatly reduced chemotactic responses to hog gastric mucin. Neither cheY1 nor cheAY2 mutants were able to colonize mice, but they generated a significant antibody response, suggesting that despite impaired chemotaxis, these mutants were able to survive in the stomach long enough to induce an immune response before being removed by gastric flow. Additionally, we demonstrated that cheY1 failed to colonize gnotobiotic piglets. This study demonstrates the importance of the roles of cheY1, cheY2, and cheA in motility and virulence of H. pylori.

Links

PubMed PMC97381

Keywords

Animals; Bacterial Proteins; Blood/microbiology; Chemotaxis; Enzyme-Linked Immunosorbent Assay; Escherichia coli/metabolism; Female; Flagella/genetics; Gastric Mucosa/microbiology; Helicobacter pylori/enzymology; Helicobacter pylori/genetics; Helicobacter pylori/pathogenicity; Membrane Proteins/genetics; Membrane Proteins/physiology; Mice; Movement; Mutagenesis, Site-Directed; Swine; Virulence

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

HELPX:I0ZC23

involved_in

GO:0052116: chemotaxis in host environment

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

HELPX:I0ZC23

GO:0052116: chemotaxis in host environment

ECO:0000315:

P

Table 3 shows a significant loss of chemotaxis function in the CheY1 and CheY2 mutants

complete
CACAO 9857

HELPX:I0ZHF1

involved_in

GO:0052116: chemotaxis in host environment

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

HELPX:I0ZHF1

GO:0052116: chemotaxis in host environment

ECO:0000315:

P

Table 3 shows significantly reduced chemotaxis in CheA mutants.

complete
CACAO 10013

See also

References

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