Analysis of the Vibrio pathogenicity island-encoded Mop protein suggests a pleiotropic role in the virulence of epidemic Vibrio cholerae

Epidemic Vibrio cholerae contain a large essential virulence gene cluster called the Vibrio pathogenicity island (VPI). We recently reported that no in vitro difference in virulence was found in El Tor strain N16961 containing a mutation in the VPI-encoded mop gene but this mutant was hypervirulent...

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Bibliographic Details
Published in:FEMS microbiology letters 2003-08, Vol.225 (2), p.311-318
Main Authors: Zhang, Dalin, Rajanna, Chythanya, Sun, Weiyun, Karaolis, David K.R.
Format: Article
Language:English
Subjects:
Animals
Bacteriology
Biofilm
Biofilms - growth & development
Biological and medical sciences
Blotting, Western
Cell Adhesion - genetics
Cholera
Cholera Toxin - biosynthesis
Colonization
Fimbriae Proteins - biosynthesis
Fundamental and applied biological sciences. Psychology
Gene Expression
Genetic Complementation Test
Genetics
Hemolysin Proteins - biosynthesis
Intestines - microbiology
Metalloendopeptidases - biosynthesis
Metalloendopeptidases - genetics
Metalloendopeptidases - physiology
Mice
Microbiology
Mop
Movement
Mutation
Pathogenesis
Pathogenicity island
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Reverse Transcriptase Polymerase Chain Reaction
Vibrio cholerae
Vibrio cholerae - genetics
Vibrio cholerae - pathogenicity
Vibrio cholerae - physiology
Virulence
Virulence - genetics
Virulence Factors - genetics
Virulence Factors - metabolism
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Summary:Epidemic Vibrio cholerae contain a large essential virulence gene cluster called the Vibrio pathogenicity island (VPI). We recently reported that no in vitro difference in virulence was found in El Tor strain N16961 containing a mutation in the VPI-encoded mop gene but this mutant was hypervirulent and reactogenic in rabbit ileal loops. In this paper, we report in vitro studies showing that independent Mop mutants of strain 3083 are significantly attenuated (∼40-fold) in cholera toxin (CT) production and have significantly increased motility and biofilm forming ability but appear to be unaffected in TcpA, hemagglutinin protease and hemolysin compared to their parent. The 3083 Mop mutant showed a 100-fold decrease in its in vivo intestinal colonization ability in the infant mouse competition assays. While reverse transcription polymerase chain reaction and phenotypic studies of a mop plasmid in both mutant and wild-type backgrounds suggest Mop is expressed by the plasmid, the differences in CT and biofilm formation could not be restored in any of the mutants. The inability to complement the Mop mutants in trans may be due either to the selection of secondary mutations or to mop possibly being part of an operon. Our findings that Mop is associated with CT, motility, biofilm formation and intestinal colonization support a hypothesis in which Mop has a pleiotropic role in the pathogenesis and persistence of epidemic V. cholerae.
ISSN:0378-1097
1574-6968
DOI:10.1016/S0378-1097(03)00535-4