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PMID:8039935

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Citation

Tsuda, M, Karita, M, Morshed, MG, Okita, K and Nakazawa, T (1994) A urease-negative mutant of Helicobacter pylori constructed by allelic exchange mutagenesis lacks the ability to colonize the nude mouse stomach. Infect. Immun. 62:3586-9

Abstract

The urease of Helicobacter pylori has been proposed to be one of its pathogenic factors. A kanamycin resistance determinant was inserted in a cloned urease gene, and transformation-mediated allelic exchange mutagenesis was carried out to introduce the disrupted gene into the corresponding wild-type chromosomal region of a clinical isolate of H. pylori, CPY3401. The resulting mutant, HPT73, had the null activity of urease. Nude mouse stomachs were challenged with these two isogenic strains to examine the role of urease in pathogenesis. Gastritis was found in the CPY3401-challenged stomachs, from which bacteria indistinguishable from CPY3401 were recovered. There was no gastritis in the HPT73-challenged stomachs, and we could not recover H. pylori from them. These results indicated that H. pylori urease is essential for colonizing the nude mouse stomach.

Links

PubMed PMC303000

Keywords

Alleles; Animals; Helicobacter pylori/enzymology; Helicobacter pylori/genetics; Helicobacter pylori/pathogenicity; Mice; Mice, Nude; Mutation; Stomach/microbiology; Urease/genetics; Urease/physiology

Significance

Annotations

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

HELPX:Q6UK76

GO:0009405: pathogenesis

ECO:0000315:

P

Table 1. Shows that strain HPT73, transformed by plasmid pHPT54 that includes a disruption of ureB gene by kanamycin resistance determinant insertion, had significantly reduced ability to colonize nude mouse stomach.

complete
CACAO 5352

HELPX:Q6UK76

involved_in

GO:0009405: pathogenesis

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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