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dc.contributor.authorRathbun, Kimberly M
dc.contributor.authorHall, Johanna E
dc.contributor.authorThompson, Stuart A
dc.date.accessioned2010-09-24T22:03:20Z
dc.date.available2010-09-24T22:03:20Z
dc.date.issued2009-08-31en_US
dc.identifier.citationBMC Microbiol. 2009 Aug 8; 9:160en_US
dc.identifier.issn1471-2180en_US
dc.identifier.pmid19664234en_US
dc.identifier.doi10.1186/1471-2180-9-160en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/106
dc.description.abstractBACKGROUND: Campylobacter jejuni is a gastrointestinal pathogen of humans, but part of the normal flora of poultry, and therefore grows well at the respective body temperatures of 37 degrees C and 42 degrees C. Proteomic studies on temperature regulation in C. jejuni strain 81-176 revealed the upregulation at 37 degrees C of Cj0596, a predicted periplasmic chaperone that is similar to proteins involved in outer membrane protein folding and virulence in other bacteria. RESULTS: The cj0596 gene was highly conserved in 24 strains and species of Campylobacter, implying the importance of this gene. To study the role that Cj0596 plays in C. jejuni pathogenesis, a mutant derivative of strain 81-176 was constructed in which the cj0596 gene was precisely deleted. A revertant of this mutant was isolated by restoring the gene to its original chromosomal location using streptomycin counterselection. The cj0596 mutant strain demonstrated a slightly decreased growth rate and lower final growth yield, yet was more motile and more invasive of human intestinal epithelial cells than wild-type. In either single or mixed infections, the mutant was less able to colonize mice than 81-176. The cj0596 mutant also expressed altered levels of several proteins. CONCLUSION: Mutation of cj0596 has an effect on phenotypes related to C. jejuni pathogenesis, probably due to its role in the proper folding of critical outer membrane proteins.
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshBacterial Proteins / genetics / metabolismen_US
dc.subject.meshCampylobacter Infections / microbiologyen_US
dc.subject.meshCampylobacter jejuni / enzymology / genetics / pathogenicityen_US
dc.subject.meshCell Lineen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Deletionen_US
dc.subject.meshHumansen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred BALB Cen_US
dc.subject.meshPeptidylprolyl Isomerase / genetics / metabolismen_US
dc.subject.meshPeriplasmic Proteins / genetics / metabolismen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshProteome / metabolismen_US
dc.titleCj0596 is a periplasmic peptidyl prolyl cis-trans isomerase involved in Campylobacter jejuni motility, invasion, and colonization.en_US
dc.typeJournal Articleen_US
dc.typeResearch Support, N.I.H., Extramuralen_US
dc.identifier.pmcidPMC2782263en_US
dc.contributor.corporatenameDepartment of Biochemistry and Molecular Biologyen_US
refterms.dateFOA2019-04-09T16:19:46Z
html.description.abstractBACKGROUND: Campylobacter jejuni is a gastrointestinal pathogen of humans, but part of the normal flora of poultry, and therefore grows well at the respective body temperatures of 37 degrees C and 42 degrees C. Proteomic studies on temperature regulation in C. jejuni strain 81-176 revealed the upregulation at 37 degrees C of Cj0596, a predicted periplasmic chaperone that is similar to proteins involved in outer membrane protein folding and virulence in other bacteria. RESULTS: The cj0596 gene was highly conserved in 24 strains and species of Campylobacter, implying the importance of this gene. To study the role that Cj0596 plays in C. jejuni pathogenesis, a mutant derivative of strain 81-176 was constructed in which the cj0596 gene was precisely deleted. A revertant of this mutant was isolated by restoring the gene to its original chromosomal location using streptomycin counterselection. The cj0596 mutant strain demonstrated a slightly decreased growth rate and lower final growth yield, yet was more motile and more invasive of human intestinal epithelial cells than wild-type. In either single or mixed infections, the mutant was less able to colonize mice than 81-176. The cj0596 mutant also expressed altered levels of several proteins. CONCLUSION: Mutation of cj0596 has an effect on phenotypes related to C. jejuni pathogenesis, probably due to its role in the proper folding of critical outer membrane proteins.


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