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Comparative Genome Analysis of Ureaplasma parvum Clinical Isolates

ABSTRACT: Ureaplasma are widespread parasites colonizing the mucosal surface of the human urogenital tract, and it has been suspected as a causative agent of nongonococcal urethritis, pregnancy complications and prenatal infections. Ureaplasma may also cause central nervous system infections and affect the lower respiratory tract of newborn babies. However, Ureaplasma spp. have also been detected in the urogenital tracts of clinically healthy patients, and their role in the development of infections thus remains unclear. Like in other organisms, virulence of Ureaplasma is determined by the presence of virulence factors - adhesions, human IgA protease, phospholipase and urease. However, the existence of interrelationships between the presence of these genes in the Ureaplasma genome and the incidence of diseases in man has not been demonstrated. Difficulties in the elucidation of these interrelationships may arise from significant macro- (gene mutation, chromosomal rearrangements) and micro- (nucleotide polymorphism) genomic heterogeneity. It is possible that the combination of the variable strain-specific genes in Ureaplasma with generally known virulence factors determine the development of pathological processes on the mucosal surface of the human urogenital tract. Keywords: macroarray, variability of genome, Ureaplasma parvum

ORGANISM(S): Ureaplasma parvum

PROVIDER: GSE5378 | GEO | 2006/07/25

SECONDARY ACCESSION(S): PRJNA96283

REPOSITORIES: GEO

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Project description:Catheter-associated urinary tract infections (CAUTIs) account for over 30% of acute nosocomial infections in the U.S. and generate $340 million in healthcare costs annually. A major causative agent of CAUTIs is Proteus mirabilis, an understudied Gram-negative pathogen noted for its ability to form urinary stones via the activity of urease. Urease mutants cannot induce stones and are attenuated in a murine UTI model, indicating this enzyme is essential to P. mirabilis pathogenesis. The ability to induce urinary stone formation requires an active urease, a nickel metalloenzyme that hydrolyzes urea. This reaction produces ammonia as a byproduct, which can serve as a nitrogen source and weak base that raises the local pH. The resulting alkalinity induces the precipitation of polyvalent cations and anions to form stones. Expression of urease genes is activated by transcriptional regulator UreR in a urea-dependent manner. Thus, urease genes are highly expressed in the urinary tract where urea is abundant (~400 mM in human urine). Production of mature urease also requires the import of nickel into the cytoplasm and its incorporation into the urease apoenzyme. Urease accessory proteins primarily acquire nickel from the Ynt transporter and facilitate the incorporation of nickel to form mature urease. P. mirabilis encodes a second, low-affinity transport system (Nik) that can provide nickel when this metal is abundant. In this study, we identified UreR as the first defined regulator of nickel transport in P. mirabilis. We also offer evidence for direct regulation of the ynt promoter by UreR. Using bioinformatics, we identified UreR-regulated urease loci in 15 Morganellaceae family species across three genera. Additionally, we located two mobilized UreR-regulated urease loci that also encode the ynt transporter, implying that UreR regulation of ynt is a conserved regulatory relationship. Our study demonstrates that UreR regulates all genes required to produce mature urease, an essential virulence factor for P. mirabilis uropathogenesis.

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Comparative Genome Analysis of Ureaplasma parvum Clinical Isolates

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